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Objective: To investigate the associations between data-driven dietary patterns, immune function, and incident type 2 diabetes (T2D) and the mediating effects of immune function., Methods: This study included 375,665 participants without diabetes at baseline in the UK Biobank study. Dietary patterns were derived through principal component analysis of food frequency questionnaire data. Immune function was assessed using 14 individual inflammatory markers and an integrated low-grade inflammation score (INFLA-score). Cox proportional hazard models were used to estimate the associations of dietary patterns or immune function with incident T2D. Linear regressions were used to estimate the associations of dietary patterns with immune function. Mediating effects of immune function were quantified., Results: During a median 14.6-year follow-up, 13,932 participants developed T2D. Four dietary patterns were identified: prudent diet (high in whole grains, vegetables, fruits, fish), wheat/dairy/eggs restrictive diet (limiting these foods), meat-based diet (high in red/processed meat, salt), and full-cream dairy diet (preference for full cream milk or dairy products). The prudent diet was negatively (HR Q4 vs Q1 , 0.69 [95% CI, 0.65-0.72]), while the wheat/dairy/eggs restrictive diet (HR Q4 vs Q1 , 1.08 [95% CI, 1.03-1.13]), meat-based diet (HR Q4 vs Q1 , 1.12 [95% CI, 1.06-1.17]), and full-cream dairy diet (HR Q4 vs Q1 , 1.08 [95% CI, 1.03-1.12]) were positively associated with incident T2D (all p for trend ≤0.04). The prudent diet was negatively and the full-cream dairy diet was positively associated with most inflammatory markers. Most inflammatory markers, especially INFLA-score (HR, 1.18 [95% CI, 1.16-1.20]), were positively associated with incident T2D. INFLA-score mediated 13% of the association with incident T2D for the prudent diet and 34% for the full-cream dairy diet., Conclusions: This study identified four distinct dietary patterns and a range of inflammatory markers associated with incident T2D. A notable proportion of the associations between dietary patterns and T2D was mediated by immune function.

Background: Obesity is often associated with impaired immune responses, including enlarged spleen, increased inflammation, and impaired T-cell-mediated function, which may lead to increased susceptibility to infections. Bioactive compounds found in various fruits and vegetables (F&V) have been shown to have strong anti-inflammatory effects. However, few prospective studies have examined the effects of F&V on preventing obesity-associated dysregulation of immune and inflammatory responses., Objective: The objective of this was to determine the impact of different levels of a mixture of F&V incorporated in a high-fat diet (HFD) on immune function changes in a diet-induced obesity animal model., Methods: Six-wk-old male C57BL/6J mice were randomly assigned to 1 of 5 groups (n = 12/group): matched low-fat control (LF, 10% kcal fat) or HFD (45% kcal fat) supplemented with 0%, 5%, 10%, or 15% (wt/wt) freeze-dried powder of the most consumed F&V (human equivalent of 0, 3, 5-7, 8-9 servings/d, respectively) for 20 wk. Spleen weight was recorded, and the immunophenotype of splenocytes was evaluated by flow cytometry. Ex vivo splenic lymphocyte proliferation was assessed by thymidine incorporation and serum cytokines concentrations were measured by Meso Scale Discovery., Results: Mice fed the HFD exhibited significantly higher spleen weight, decreased splenic CD8+ lymphocytes, suppressed T lymphocyte proliferation, and reduced serum IL-1ß and IFN-γ concentrations compared with those fed the LF diet. Feeding mice with the HFD supplemented with 10% or 15% F&V restored HFD-associated changes of these affected biomarkers compared with those fed HFD only. Furthermore, a significant correlation was found between immunologic markers and F&V level., Conclusions: These results suggest that increased consumption of F&V has beneficial effects in preventing HFD-associated dysregulation of immune function., (Copyright © 2024 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

Background and Aims: Whole grain consumption is widely recognized as a vital component of a balanced diet. Dietary fiber has been well-documented to play a crucial role in these health benefits attributed to whole grain intake. However, population-based evidence directly linking whole grain consumption to anti-inflammatory effects, especially in the context of immune-mediated inflammation, remains limited. We hypothesized that whole grain consumption promotes health by modulating immune-mediated inflammation., Methods and Results: This study was designed as a real-world, population-based randomized controlled trial. We compared the effects of whole grain versus refined grain consumption on immune-mediated inflammation through staple food substitution, while participants maintained their usual dietary practices. The results demonstrated that whole grain consumption significantly reduced circulating levels of pro-inflammatory cytokines IL-22 and IL-23 compared to refined grain consumption. These reductions were associated with optimized short-chain fatty acid profiles and changes in CD4 + T cell subset distributions., Conclusions: The findings suggest that the anti-inflammatory effects of whole grain consumption in middle-aged and elderly populations are mediated by targeting specific CD4 + T cell subsets, in addition to modulating both upstream short-chain fatty acid composition and downstream expression of the pro-inflammatory cytokines IL-22 and IL-23., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Purpose of Review: The aim of this systematic review was to investigate the effects of whole grain Avena sativa and Hordeum vulgare L., or their isolated fractions, on immune and inflammatory functions, as well as their influence on gut microbiota. A structured literature search was undertaken in line with PRISMA guidelines. Randomized controlled trials (RCTs) that investigated the effects of oats or barley consumption in adults and reported ≥ 1 of the following: C-reactive protein (CRP), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), IL-2, IL-8, IL-18, lipopolysacharide binding protein (LBP) or gut microbiota-related outcomes, were included., Recent Findings: A total of 16 RCTs were included, among which 6 studies recruited metabolically at-risk population, including individuals with overweight and obesity, metabolic syndrome or hypercholesterolemia. Additionally, 3 trials involved young healthy population, 5 trials targeted older individuals (aged over 50 years), and 2 studies encompassed populations with other disease states. A total of 1091 individuals were included in the evaluation of short-term (up to 14 days) and long-term (beyond 14 days, up to 90 days) supplementation with oats or barley-based products. 9 studies measured inflammatory biomarkers and 5 of them reported significant reductions, specifically in long-term studies. Notably, no evidence of anti-inflammatory benefits was found in healthy individuals, whereas studies involving metabolically at-risk populations showed promising reductions in inflammation. 13 studies measured the impact on gut microbiota, and collectively suggest that oats and barley food products can influence the composition of gut microbiota, associated in some cases with metabolic improvements. Oats and barley consumption may confer anti-inflammatory effects in metabolically at-risk populations and influence gut microbiota outcomes. However, no anti-inflammatory benefits were observed in healthy individuals. Results from this systematic review suggests caution in interpreting findings due to limited trials and variations in interventions and health conditions., (© 2024. The Author(s).)

Mycoplasma gallisepticum (MG) can cause chronic respiratory disease (CRD) in chickens, which has a significant negative economic impact on the global poultry sector. Respiratory flora is the guardian of respiratory health, and its disorder is closely related to respiratory immunity and respiratory diseases. As a common probiotic in the chicken respiratory tract, Lactobacillus salivarius (L. salivarius) has potential antioxidant, growth performance enhancing, and anti-immunosuppressive properties. However, the specific mechanism through which L. salivarius protects against MG infection has not yet been thoroughly examined. This study intends to investigate whether L. salivarius could reduce MG-induced tracheal inflammation by modulating the respiratory microbiota and metabolites. The results indicated that L. salivarius reduced MG colonization significantly and alleviated the anomalous morphological changes by using the MG-infection model. L. salivarius also reduced the level of Th1 cell cytokines, increased the level of Th2 cell cytokines, and ameliorated immune imbalance during MG infection. In addition, L. salivarius improved the mucosal barrier, heightened immune function, and suppressed the Janus kinase/Signal transducer, and activator of transcription (JAK/STAT) signaling pathway. Notably, MG infection changed the composition of the respiratory microbiota and metabolites, and L. salivarius therapy partially reversed the aberrant respiratory microbiota and metabolite composition. Our results highlighted that these findings demonstrated that L. salivarius played a role in MG-mediated inflammatory damage and demonstrated that L. salivarius, by altering the respiratory microbiota and metabolites, could successfully prevent MG-induced inflammatory injury in chicken trachea., Competing Interests: DISCLOSURES The authors declare no conflicts of interest., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Chronic Obstructive Pulmonary Disease (COPD) progression in the elderly is notably influenced by nutritional, immune, and inflammatory status. This study aimed to investigate the impact of adequate energy supply on these indicators in COPD patients., Methods: COPD patients meeting specific criteria were recruited and categorized into energy-adequate and energy-deficient groups based on their energy supply. Comparable demographic factors such as age, gender, smoking and drinking history, COPD duration, inhaled drug classification, and home oxygen therapy application were observed. Notable differences were found in BMI and inhaled drug use between the two groups., Results: The energy-adequate group exhibited significant improvements in various health indicators, including lymphocyte count, hemoglobin, CRP, total cholesterol, prealbumin, albumin, PNI, SII, SIRI, CAR, and CONUT scores in the secondary auxiliary examination. These positive changes suggest a notable enhancement in nutritional, immune, and inflammatory status., Conclusion: This research highlights the substantial benefits of adequate energy supply in elderly COPD patients. The observed improvements in nutritional, immune, and inflammatory markers underscore the importance of addressing energy needs to positively influence disease-related outcomes in this population. These findings have implications for developing targeted interventions to optimize the well-being of elderly individuals with COPD., Competing Interests: The authors declare no competing interest in this work., (© 2024 Gao et al.)

Understanding sex differences in immunological responses in the context of obesity is important to improve health outcomes. This systematic review aimed to investigate sex differences in systemic inflammation, immune cell phenotype, and function in diet-induced obesity (DIO) animal models. A systematic search in Medline, Embase, and CINAHL from inception to April 2023 was conducted, using a combination of the following concepts: sex, obesity, cytokines, and immune cell phenotypes/function. Forty-one publications reporting on systemic inflammation (61%), cell phenotype (44%), and/or function (7%) were included. Females had lower systemic inflammation compared with males in response to DIO intervention and a higher proportion of macrophage (M)2-like cells compared with males that had a higher proportion of M1-like in adipose tissue. Although there were no clear sex differences in immune function, high-fat DIO intervention remains an important factor in the development of immune dysfunction in both males and females, including disturbances in cytokine production, proliferation, and migration of immune cells. Yet, the mechanistic links between diet and obesity on such immune dysfunction remain unclear. Future studies should investigate the role of diet and obesity in the functionality of immune cells and employ adequate methods for a high-quality investigation of sex differences in this context., (© 2023 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation.)

Aim: Angiotensin-converting enzyme 2 (ACE 2) is the binding domain for severe acute respiratory syndrome coronavirus (SARS-CoV) and SARSCoV-2. Some antihypertensive drugs affect ACE2 expression or activity (ACE inhibitors and angiotensin II receptor blockers [ARBs]), suggesting use of other hypertensives might be preferable, such as calcium channel blockers (CCBs). Given the limited evidence, the International Society of Hypertension does not support such a policy., Methods: We used a Mendelian randomization study to obtain unconfounded associations of antihypertensives, instrumented by published genetic variants in genes regulating target proteins of these drugs, with immune (lymphocyte and neutrophil percentage) and inflammatory (tumour necrosis factor alpha [TNF-α]) markers in the largest available genome-wide association studies., Results: Genetically predicted effects of ACE inhibitors increased lymphocyte percentage (0.78, 95% confidence interval [CI] 0.35, 1.22), decreased neutrophil percentage (-0.64, 95% CI -1.09, -0.20) and possibly lowered TNF-α (-4.92, 95% CI -8.50, -1.33). CCBs showed a similar pattern for immune function (lymphocyte percentage 0.21, 95% CI 0.05 to 0.36; neutrophil percentage -0.23, 95% CI -0.39 to -0.08) but had no effect on TNF-α, as did potassium-sparing diuretics and aldosterone antagonists, and vasodilator antihypertensives. ARBs and other classes of hypertensives had no effect on immune function or TNF-α., Conclusion: Varying effects of different classes of antihypertensives on immune and inflammatory markers do not suggest antihypertensive use based on their role in ACE2 expression, but instead suggest investigation of the role of antihypertensives in immune function and inflammation might reveal important information that could optimize their use in SARSCoV-2., (© 2020 British Pharmacological Society.)

Background: Lung cancer-related inflammation is associated with depression. Both elevated inflammation and depression are associated with worse survival. However, outcomes of patients with concomitant depression and elevated inflammation are not known. Materials & methods: Patients with metastatic lung cancer (n = 123) were evaluated for depression and inflammation. Kaplan-Meier plots and Cox proportional hazard models provided survival estimations. Results: Estimated survival was 515 days for the cohort and 323 days for patients with depression (hazard ratio: 1.12; 95% CI: 1.05-1.179), 356 days for patients with elevated inflammation (hazard ratio: 2.85, 95% CI: 1.856-4.388), and 307 days with both (χ 2  = 12.546; p < 0.001]). Conclusion: Depression and inflammation are independently associated with inferior survival. Survival worsened by inflammation is mediated by depression-a treatable risk factor.

This study aimed to verify the efficacy of a combined treatment of Jakyakgamcho-tang (JGT) and acupuncture (CV12, ST25, CV4) on colitis induced by dextrane sulfate sodium (DSS). Changes in immuno-mediated factors and metabolites were investigated. Colitis symptoms such as body weight loss and elevated disease activity index were alleviated by the combined treatment. Moreover, treatment with JGT and acupuncture restored the disturbed architecture of colon by suppressing inflammatory cytokine levels of IFN-[Formula: see text] ([Formula: see text] < 0.05), IL-5 ([Formula: see text] < 0.05), and IL-13 ([Formula: see text] < 0.0001) compared with the DSS group. Analysis of metabolic profiles of serum revealed that treatment groups were clearly separated from the DSS group, suggesting that JGT and acupuncture treatment altered serum metabolites. Furthermore, treatments caused opposite metabolite patterns for dimethylbenzimidazole, 1,5-anhydro-D-glucitol, proline, phosphate, glycolic acid, aspartic acid, tryptophan, phthalic acid, ornithine, and glutamic acid compared with the DSS group. The combined treatment group induced more effective metabolite patterns than the JGT group, implying that acupuncture treatment can restore metabolic changes caused by DSS induction. These results indicate that the simultaneous treatment of JGT administration and acupuncture procedure provides better management of the immune function and inflammatory expression of colitis than a single treatment. It is assumed that intestinal microbial control can be achieved by acupuncture stimulation as well as by taking herbal medicine.

Post-stroke systemic inflammation, due to the injury itself and exacerbated by in-hospital infections, can increase morbidity and mortality in stroke patients. In this study, we examined the immunomodulatory effects of progesterone (P4) alone and in combination with vitamin D hormone (VDH) on acute phase post-stroke peripheral immune dysfunction and functional/behavioral deficits. Adult rats underwent transient middle cerebral artery occlusion/reperfusion (tMCAO) and delayed systemic inflammation was induced by injections of lipopolysaccharide (LPS) beginning 24 h post-stroke. Animals were tested for behavioral outcomes and immune function at day 4 post-stroke. We also measured infarction volume and markers of neuronal inflammation (GFAP, IL-6) and apoptosis (cleaved caspase-3) in brain post-stroke. We observed the worst stroke outcomes in the stroke + systemic inflammation group compared to the stroke-alone group. Flow cytometric analysis of different subsets of immune cells in blood, spleen and thymus revealed peripheral immune dysfunction which was restored by both P4 and VDH monotherapy. P4 monotherapy reduced infarction volume, behavioral/functional deficits, peripheral immune dysfunction, neuronal inflammation, and apoptosis induced by post-stroke systemic inflammation. Combination treatment with P4+VDH improved outcomes better than monotherapy. Our findings can be taken to suggest that the current standard of care for stroke and post-stroke infection can be substantially improved by P4 and VDH combination therapy., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

As the most dominant cell type in the skin, keratinocytes play critical roles in wound repair not only as structural cells but also exerting important immune functions. This review focuses on the communications between keratinocytes and immune cells in wound healing, which are mediated by various cytokines, chemokines, and extracellular vesicles. Keratinocytes can also directly interact with T cells via antigen presentation. Moreover, keratinocytes produce antimicrobial peptides that can directly kill the invading pathogens and contribute to wound repair in many aspects. We also reviewed the epigenetic mechanisms known to regulate keratinocyte immune functions, including histone modifications, non-protein-coding RNAs (e.g., microRNAs, and long noncoding RNAs), and chromatin dynamics. Lastly, we summarized the current evidence on the dysregulated immune functions of keratinocytes in chronic nonhealing wounds. Based on their crucial immune functions in skin wound healing, we propose that keratinocytes significantly contribute to the pathogenesis of chronic wound inflammation. We hope this review will trigger an interest in investigating the immune roles of keratinocytes in chronic wound pathology, which may open up new avenues for developing innovative wound treatments.

This study aimed to investigate the effects of a short-term (36 h) fasting period combined with an acute bout of exercise on markers of immune function and inflammation in healthy human subjects. Fourteen moderately trained male subjects (aged 19-39 yr) participated in a 36-h fasting trial (FA-T), followed by an acute bout of moderate exercise (60% V̇o 2max ). After 1 wk, the same subjects, as their own control, participated in a nonfasting trial (NFA-T) in which they performed an exercise trial of the same duration and intensity. Blood samples were taken before, immediately after, and 1 h after each exercise bout and analyzed for several immunological and metabolic markers. At baseline, fasting subjects showed lower levels of T cell apoptosis, lymphocyte-proliferative responses, IL-6, monocyte chemoattractant protein-1 (MCP-1), insulin, and leptin ( P < 0.05) as well as higher levels of neutrophil oxidative burst and thiobarbituric acid reactive substances (TBARS) than those in the NFA-T ( P < 0.05). After the exercise protocol, fasted subjects revealed higher T cell apoptosis, neutrophil oxidative burst, TBARS, TNFα, and MCP-1 levels as well as lower levels of lymphocyte-proliferative response, IL-6, insulin, and leptin than those in the NFA-T ( P < 0.05). Short-term fasting aggravates perturbations in markers of immune function, and inflammation was induced by an acute moderate-intensity exercise protocol.

The long-standing interest in the effects of religiosity and spirituality (R/S) on health outcomes has given rise to a large and diverse literature. We conducted a meta-analysis on research involving R/S and physiological markers of health to elucidate both the scope and mechanism(s) of this phenomenon. A combined analysis found a significant, but small, beneficial effect. Subgroup analyses found that some measures of both extrinsic and intrinsic religiosity were significantly associated with health. Several outcome measures, including blood pressure, C-reactive protein, and cardiovascular health markers, were significantly associated with R/S. Our findings suggest that R/S benefits health, perhaps through minimizing the disruptive effects of stress/depression on inflammation. We hope that researchers can use these results to guide efforts aimed at elucidating the true mechanism(s) linking religious/spiritual beliefs and physical health.

Enhancing the supply of arginine (Arg), a semi-essential amino acid, has positive effects on immune function in dairy cattle experiencing metabolic stress during early lactation. Our objective was to determine the effects of Arg supplementation on biomarkers of liver damage and inflammation in cows during early lactation. Six Chinese Holstein lactating cows with similar BW (508 ± 14 kg), body condition score (3.0), parity (4.0 ± 0), milk yield (30.6 ± 1.8 kg) and days in milk (20 ± days) were randomly assigned to three treatments in a replicated 3 × 3 Latin square design balanced for carryover effects. Each period was 21 days with 7 days for infusion and 14 days for washout. Treatments were (1) Control: saline; (2) Arg group: saline + 0.216 mol/day l-Arg; and (3) Alanine (Ala) group: saline + 0.868 mol/day l-Ala (iso-nitrogenous to the Arg group). Blood and milk samples from the experimental cows were collected on the last day of each infusion period and analyzed for indices of liver damage and inflammation, and the count and composition of somatic cells in milk. Compared with the Control, the infusion of Arg led to greater concentrations of total protein, immunoglobulin M and high density lipoprotein cholesterol coupled with lower concentrations of haptoglobin and tumor necrosis factor-α, and activity of aspartate aminotransferase in serum. Infusion of Ala had no effect on those biomarkers compared with the Control. Although milk somatic cell count was not affected, the concentration of granulocytes was lower in response to Arg infusion compared with the Control or Ala group. Overall, the biomarker analyses indicated that the supplementation of Arg via the jugular vein during early lactation alleviated inflammation and metabolic stress.

Extracellular vesicles (EVs) are blebs of either plasma membrane or intracellular membranes carrying a cargo of proteins, nucleic acids, and lipids. EVs are produced by eukaryotic cells both under physiological and pathological conditions. Genetic and environmental factors (diet, stress, etc.) affecting EV cargo, regulating EV release, and consequences on immunity will be covered. EVs are found in virtually all body fluids such as plasma, saliva, amniotic fluid, and breast milk, suggesting key roles in immune development and function at different life stages from in utero to aging. These will be reviewed here. Under pathological conditions, plasma EV levels are increased and exacerbate immune activation and inflammatory reaction. Sources of EV, cells targeted, and consequences on immune function and disease development will be discussed. Both pathogenic and commensal bacteria release EV, which are classified as outer membrane vesicles when released by Gram-negative bacteria or as membrane vesicles when released by Gram-positive bacteria. Bacteria derived EVs can affect host immunity with pathogenic bacteria derived EVs having pro-inflammatory effects of host immune cells while probiotic derived EVs mostly shape the immune response towards tolerance.

Diet is major modifiable risk factor for cardiovascular disease that can influence the immune status of the individual and contribute to persistent low-grade inflammation. In recent years, there has been an increased appreciation of the role of polyunsaturated fatty acids (PUFA) in improving immune function and reduction of systemic inflammation via the modulation of pattern recognition receptors (PRR) on immune cells. Extensive research on the use of bioactive lipids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and their metabolites have illustrated the importance of these pro-resolving lipid mediators in modulating signaling through PRRs. While their mechanism of action, bioavailability in the blood, and their efficacy for clinical use forms an active area of research, they are found widely administered as marine animal-based supplements like fish oil and krill oil to promote health. The focus of this review will be to discuss the effect of these bioactive fatty acids and their metabolites on immune cells and the resulting inflammatory response, with a brief discussion about modern methods for their analysis using mass spectrometry-based methods.

Background: Dexmedetomidine (DEX) is a highly selective alpha2 adrenoceptor agonist with broad pharmacological effects, including sedation, analgesia, anxiolysis, and sympathetic tone inhibition. Here we report a systematic review and meta-analysis of its effects on stress, inflammation, and immunity in surgical patients during the perioperative period., Methods: We searched MEDLINE, METSTR, Embase, and Web of Science for clinical studies or trials to analyse the effects of DEX on perioperative stress, inflammation, and immune function., Results: Sixty-seven studies (including randomised controlled trials and eight cohort studies) with 4842 patients were assessed, of which 2454 patients were in DEX groups and 2388 patients were in control (without DEX) groups. DEX infusion during the perioperative period inhibited release of epinephrine, norepinephrine, and cortisol; decreased blood glucose, interleukin (IL)-6, tumour necrosis factor-α, and C-reactive protein; and increased interleukin-10 in surgical patients. In addition, the numbers of natural killer cells, B cells, and CD4 + T cells, and the ratios of CD4 + :CD8 + and Th1:Th2 were significantly increased; CD8 + T-cells were decreased in the DEX group when compared with the control group., Conclusions: DEX, an anaesthesia adjuvant, can attenuate perioperative stress and inflammation, and protect the immune function of surgical patients, all of which may contribute to decreased postoperative complications and improved clinical outcomes., (Copyright © 2019 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.)

Background: To investigate the effects of dual plasma molecular adsorption system (DPMAS) on the liver function, electrolytes, inflammation, and immunity in patients with chronic severe hepatitis (CSH)., Methods: Total of 162 patients with CSH treated in our hospital from March 2016 to December 2018 were enrolled and equally randomly divided into control group (n = 81) and observation group (n = 81). The patients in control group were treated with plasma exchange, while those in observation group were additionally treated with DPMAS based on the treatment in control group. The liver function, electrolytes, inflammation, and immunity were evaluated and compared between the two groups., Results: After treatment, the liver function indexes in observation group were significantly favorable compared with those in control group, with the reduction in TBIL, DBIL, ALT, and rise of CHE levels (P < 0.05). The levels of K + , Na + , Cl - , and Ca 2+ in both groups were significantly improved after treatment (P < 0.05), although there were no significant differences between the two groups (P > 0.05). The levels of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in both groups declined after treatment compared with those before treatment, and those levels in observation group were higher than that in control group (P < 0.05). After treatment, the levels of cluster of differentiation 3 + (CD3 + ), CD4 + , and CD4 + /CD8 + were higher in observation group than those in control group, with decreasing level of CD8 + (P < 0.05)., Conclusion: Dual plasma molecular adsorption system can effectively improve the liver function, effectively correct the electrolyte disorders, reduce the inflammatory response, and adjust the immunity in patients with CSH., (© 2019 The Authors Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc.)

Vitamin E, a potent lipid-soluble antioxidant, found in higher concentration in immune cells compared to other cells in blood, is one of the most effective nutrients known to modulate immune function. Vitamin E deficiency has been demonstrated to impair normal functions of the immune system in animals and humans, which can be corrected by vitamin E repletion. Although deficiency is rare, vitamin E supplementation above current dietary recommendations has been shown to enhance the function of the immune system and reduce risk of infection, particularly in older individuals. The mechanisms responsible for the effect of vitamin E on the immune system and inflammation have been explored in cell-based, pre-clinical and clinical intervention studies. Vitamin E modulates T cell function through directly impacting T cell membrane integrity, signal transduction, and cell division, and also indirectly by affecting inflammatory mediators generated from other immune cells. Modulation of immune function by vitamin E has clinical relevance as it affects host susceptibility to infectious diseases such as respiratory infections, in addition to allergic diseases such as asthma. Studies examining the role of vitamin E in the immune system have typically focused on α-tocopherol; however, emerging evidence suggests that other forms of vitamin E, including other tocopherols as well as tocotrienols, may also have potent immunomodulatory functions. Future research should continue to identify and confirm the optimal doses for individuals at different life stage, health condition, nutritional status, and genetic heterogeneity. Future research should also characterize the effects of non-α-alpha-tocopherol vitamin E on immune cell function as well as their potential clinical application. © 2018 IUBMB Life, 71(4):487-494, 2019., (© 2018 International Union of Biochemistry and Molecular Biology.)

Air pollution is known to increase the risk of pneumonia. However, the effects of air pollution on the pleural effusion of patients with pneumonia are unclear. The objective of this study was to investigate alterations in inflammatory⁻immune biomarkers by air pollution in patients with pneumonia by analyzing their pleural effusion. Patients who had undergone thoracentesis to drain their pleural effusion in a hospital were recruited for this study. Patients with pneumonia and those with congestive heart failure respectively served as the case and control groups. We observed that an increase of 1 ppb in one-year NO₂ was associated with a decrease of 0.105 ng/mL in cluster of differentiation 62 (CD62) (95% confidence interval (CI) = -0.085, -0.004, p < 0.05) in the pleural effusion. Furthermore, we observed that an increase in one-year 1 ppb of NO₂ was associated with a decrease of 0.026 ng/mL in molybdenum (Mo) (95% CI = -0.138, -0.020, p < 0.05). An increase in one-year 1 ppb of SO₂ was associated with a decrease of 0.531 ng/mL in zinc (95% CI = -0.164, -0.006, p < 0.05). Also, an increase in one-year 1 ppb of O₃ was associated with a decrease of 0.025 ng/mL in Mo (95% CI = -0.372, -0.053, p < 0.05). In conclusion, air pollution exposure, especially gaseous pollution, may be associated with the regulation of immune responses and changes in metal levels in the pleural effusion of pneumonia patients.

Purpose of Review: Tobacco use, sex differences, and psychiatric disorders are associated with altered immune function. There are also sex differences in tobacco use and psychiatric disorders. This review summarizes findings from the small, but growing literature examining sex differences in the effects of tobacco use on inflammation and the implications for psychiatric disorders., Recent Findings: We identified four studies that tested the interaction between sex and tobacco/nicotine on inflammation. Although males and females generally exhibited differential tobacco-induced immune responses, the pattern varied depending on the sample (rodents vs. humans) and the method to evaluate inflammation. Evidence suggests that sex modulates the effects of tobacco smoke on inflammation. Many inflammation markers associated with sex differences and tobacco use are related to psychiatric disorders. We propose a model in which sex, tobacco use, and inflammation interact to increase risk for psychiatric disorders. Future studies are needed to examine the mechanisms that explain this relationship.

Patients with a diagnosis of multiple sclerosis (MS) or major depressive disorder (MDD) share a wide array of biological abnormalities which are increasingly considered to play a contributory role in the pathogenesis and pathophysiology of both illnesses. Shared abnormalities include peripheral inflammation, neuroinflammation, chronic oxidative and nitrosative stress, mitochondrial dysfunction, gut dysbiosis, increased intestinal barrier permeability with bacterial translocation into the systemic circulation, neuroendocrine abnormalities and microglial pathology. Patients with MS and MDD also display a wide range of neuroimaging abnormalities and patients with MS who display symptoms of depression present with different neuroimaging profiles compared with MS patients who are depression-free. The precise details of such pathology are markedly different however. The recruitment of activated encephalitogenic Th17 T cells and subsequent bidirectional interaction leading to classically activated microglia is now considered to lie at the core of MS-specific pathology. The presence of activated microglia is common to both illnesses although the pattern of such action throughout the brain appears to be different. Upregulation of miRNAs also appears to be involved in microglial neurotoxicity and indeed T cell pathology in MS but does not appear to play a major role in MDD. It is suggested that the antidepressant lofepramine, and in particular its active metabolite desipramine, may be beneficial not only for depressive symptomatology but also for the neurological symptoms of MS. One clinical trial has been carried out thus far with, in particular, promising MRI findings.

Background: Aging is characterized with immunosenescence associated with a hyper-inflammatory state, characterized by elevated circulating levels of pro-inflammatory mediators. Physical exercise is a potential strategy for improving the immune system dysfunction and chronic inflammation that accompanies aging. However, there is a need to differentiate between aerobic and resistance exercise training regarding human immune system and systemic inflammation among the elderly Saudi population., Objective: The aim of this study was to compare the impact of 6 months of aerobic versus resisted exercise training on inflammatory cytokines and immune system response among elderly., Material and Methods: Sixty previously sedentary elderly subjects participated in this study, their age ranged from 61-66 years. All Subjects were randomly assigned to supervised aerobic exercise intervention group (group A, n=40) or resistance exercise group (group B, n=40). Number of CD3 + ,CD4 + ,CD8 + T cells count and CD4/CD8 ratio were quantified, IL-6, TNF-α and IL10 were measured before and after 6 months, at the end of the study., Results: The mean values of CD3 + , CD4 + and CD8 + T cells count and IL-10 were significantly increased, whereas the mean values of CD4/CD8 ratio, IL-6 and TNF-α were significantly decreased in group (A) and group (B). Also; there were significant differences between mean levels of the investigated parameters in group (A) and group (B) after treatment., Conclusion: The current study provides evidence that aerobic exercise is more appropriate in modulating the immune system and inflammatory markers among the elderly population.

Systemic immune function is impaired by sleep restriction. However, the impact of sleep restriction on local immune responses and to what extent any impairment can be mitigated by nutritional supplementation is unknown. We assessed the effect of 72-h sleep restriction (2-h nightly sleep) on local immune function and skin barrier restoration of an experimental wound, and determined the influence of habitual protein intake (1.5 g·kg -1 ·day -1 ) supplemented with arginine, glutamine, zinc sulfate, vitamin C, vitamin D3, and omega-3 fatty acids compared with lower protein intake (0.8 g·kg -1 ·day -1 ) without supplemental nutrients on these outcomes. Wounds were created in healthy adults by removing the top layer of less than or equal to eight forearm blisters induced via suction, after adequate sleep (AS) or 48 h of a 72-h sleep restriction period (SR; 2-h nightly sleep). A subset of participants undergoing sleep restriction received supplemental nutrients during and after sleep restriction (SR+). Wound fluid was serially sampled 48 h postblistering to assess local cytokine responses. The IL-8 response of wound fluid was higher for AS compared with SR [area-under-the-curve (log 10 ), 5.1 ± 0.2 and 4.9 ± 0.2 pg/ml, respectively; P = 0.03]; and both IL-6 and IL-8 concentrations were higher for SR+ compared with SR ( P < 0.0001), suggestive of a potentially enhanced early wound healing response. Skin barrier recovery was shorter for AS (4.2 ± 0.9 days) compared with SR (5.0 ± 0.9 days) ( P = 0.02) but did not differ between SR and SR+ ( P = 0.18). Relatively modest sleep disruption delays wound healing. Supplemental nutrition may mitigate some decrements in local immune responses, without detectable effects on wound healing rate. NEW & NOTEWORTHY The data herein characterizes immune function in response to sleep restriction in healthy volunteers with and without nutrition supplementation. We used a unique skin wound model to show that sleep restriction delays skin barrier recovery, and nutrition supplementation attenuates decrements in local immune responses produced by sleep restriction. These findings support the beneficial effects of adequate sleep on immune function. Additional studies are necessary to characterize practical implications for populations where sleep restriction is unavoidable.

There is strong evidence that the immune system changes dramatically during pregnancy in order to prevent the developing fetus from being "attacked" by the maternal immune system. Due to these alterations in peripheral immune function, many women that suffer from autoimmune disorders actually find significant relief from their symptoms throughout pregnancy; however, these changes can also leave the mother more susceptible to infections that would otherwise be mitigated by the inflammatory response (Robinson and Klein, 2012). Only one other study has looked at changes in microglial number and morphology during pregnancy and the postpartum period (Haim et al., 2016), but no one has yet examined the neuroimmune response following an immune challenge during this time. Therefore, in this study, we investigated the impact of an immune challenge during various time-points throughout pregnancy and the postpartum period on the expression of immune molecules in the brain of the mother and fetus. Our results indicate that similar to the peripheral immune suppression measured during pregnancy, we also see significant suppression of the immune response in the maternal brain, particularly during late gestation. In contrast to the peripheral immune system, immune modulation in the maternal brain extends moderately into the postpartum period. Additionally, we found that the fetal immune response in the brain and placenta is also suppressed just before parturition, suggesting that cytokine production in the fetus and placenta are mirroring the peripheral cytokine response of the mother., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Quercetin (Q) and green tea extract (E) are reported to counter insulin resistance and inflammation and favorably alter fat metabolism. We investigated whether a mixture of E + Q (EQ) could synergistically influence metabolic and inflammation endpoints in a high-fat diet (HFD) fed to mice. Male C57BL/6 mice ( n = 40) were put on HFD (fat = 60%kcal) for 12 weeks and randomly assigned to Q (25 mg/kg of body weight (BW)/day), E (3 mg of epigallocatechin gallate/kg BW/day), EQ, or control groups for four weeks. At 16 weeks, insulin sensitivity was measured via the glucose tolerance test (GTT), followed by area-under-the-curve (AUC) estimations. Plasma cytokines and quercetin were also measured, along with whole genome transcriptome analysis and real-time polymerase chain reaction (qPCR) on adipose, liver, and skeletal muscle tissues. Univariate analyses were conducted via analysis of variance (ANOVA), and whole-genome expression profiles were examined via gene set enrichment. At 16 weeks, plasma quercetin levels were higher in Q and EQ groups vs. the control and E groups ( p < 0.05). Plasma cytokines were similar among groups ( p > 0.05). AUC estimations for GTT was 14% lower for Q vs. E ( p = 0.0311), but non-significant from control ( p = 0.0809). Genes for cholesterol metabolism and immune and inflammatory response were downregulated in Q and EQ groups vs. control in adipose tissue and soleus muscle tissue. These data support an anti-inflammatory role for Q and EQ, a result best captured when measured with tissue gene downregulation in comparison to changes in plasma cytokine levels., Competing Interests: The authors declare no conflict of interest.

Background: Despite recent advances in the medical and surgical fields, complications such as infection, pneumonia, or brain swelling may occur after a craniotomy. In some patients, perioperative antibiotic prophylaxis causes adverse effects such as itching, rash, or digestive conditions. Certain patients still develop infections severe enough to require a repeat operation despite antibiotic prophylaxis. Acupuncture has been used to treat inflammatory conditions, and many basic and clinical studies have provided evidence of its anti-inflammatory and immune regulatory effects. The aim of this study is to explore the effects of acupuncture on inflammation and immune function after craniotomy., Methods: This trial will be a single-center, parallel-group clinical trial. Forty patients who underwent craniotomy for an unruptured aneurysm, facial spasm, or a brain tumor will be allocated to either the study or the control group. The study group will receive conventional management as well as acupuncture, electroacupuncture, and intradermal acupuncture, which will start within 48 h of the craniotomy. The patients will receive a total of six sessions within 8 days. The control group will only receive conventional management. The primary outcome measure will be the C-reactive protein levels, while the secondary outcomes will be the serum erythrocyte sedimentation rate and the tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 levels measured at four different time points: within 48 h prior to the craniotomy and on days 2, 4, and 7 after surgery. The presence of fever and infection, the use of additional antibiotics, the presence of infection, including pneumonia or urinary tract infection, and safety will also be investigated., Discussion: In this trial, we will observe whether acupuncture has anti-inflammatory and immune regulatory effects after a craniotomy. If our study yields positive results and a placebo-controlled study also finds favorable results following our study, acupuncture could be recommended as an adjunctive therapy after a craniotomy., Trial Registration: ClinicalTrials.gov: NCT02761096 . Registered on 27 April 2016.

Aim: Fire Service Instructors (FSI) are exposed to many repeated periods of high environmental temperatures when training firefighters. Such repeated exposures will impose significant strains on the function of instructors. We aimed to measure the effects of a training programme including repeated exposures to heat, termed "Wears" in the fire service, on the physiological, psychological some immunological markers of Fire Service Instructors., Methods: Six FSI and six physiologically matched controls completed blood and cardiovascular tests pre and post a 4wk heat instruction training block, controls completed the tests only. FSI were given a 7wk period of no heat exposure prior to starting the training. Physiological and perceptual measures were taken pre and post the first and last Wear of the 4wk training protocol., Results: There were acute effects of a Wear on core temperature and physiological strain index, as well as measures of fatigue. The acute exposure to heat during a Wear led to a consistent decrease in CRP (-10% to -40%), increased IL6 concentrations 33-45%) as well as increased RPE and TSS. Over the training programme significantly lower quantities of white cells, particularly neutrophils, leukocytes and monocytes were found in the FSI group. Between the start and the end of the 4 week training programme the FSI showed a significantly greater physiological strain index (PSI) to the Wears, which nearly doubled from 2.5 to 4.7 (p<0.05)., Conclusion: Physiological and psychological measures indicate that FSI may be experiencing symptoms and changes to their health consistent with an overtraining type condition., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

In vitro and some animal models have shown that quercetin, a polyphenol derived from plants, has a wide range of biological actions including anti-carcinogenic, anti-inflammatory and antiviral activities; as well as attenuating lipid peroxidation, platelet aggregation and capillary permeability. This review focuses on the physicochemical properties, dietary sources, absorption, bioavailability and metabolism of quercetin, especially main effects of quercetin on inflammation and immune function. According to the results obtained both in vitro and in vivo, good perspectives have been opened for quercetin. Nevertheless, further studies are needed to better characterize the mechanisms of action underlying the beneficial effects of quercetin on inflammation and immunity.

The purpose of this randomized controlled trial was to determine the effects of resistance training (RT) on markers of inflammation and immune function in breast cancer survivors. Thirty-nine breast cancer survivors were randomly assigned to a RT (n = 20) or control (n = 19) group. RT performed supervized exercise three times per week. Natural killer cell (NK) and natural killer T-cell (NKT) function, and markers of inflammation (serum TNF-α, IL-6, IL-10, and CRP) were measured before and after training. Changes in NK and NKT cell function were analyzed using ANCOVA, with the change score the dependent variable, and the baseline value of the same variable the covariate. Effect sizes (ES) were calculated via partial eta-squared. We found a significant reduction, and large associated ESs, in the RT group compared to the control group for change in NK cell expression of TNF-α (p = 0.005, ES = 0.21) and NKT cell expression of TNF-α (p = 0.04, ES = 0.12). No differences were observed in any serum marker. Significant improvements in all measurements of strength were found in RT compared to control (p < 0.001; large ESs ranging from 0.32 to 0.51). These data demonstrate that RT has a beneficial effect on the NK and NKT cell expression of TNF-α indicating that RT may be beneficial in improving the inflammatory profile in breast cancer survivors.

Toll-like receptor (TLR) signaling is central to innate immunity. Aberrant expression of TLRs is found in neonatal inflammatory diseases. Several bioactive components of human milk modulate TLR expression and signaling pathways, including soluble toll-like receptors (sTLRs), soluble cluster of differentiation (sCD) 14, glycoproteins, small peptides, and oligosaccharides. Some milk components, such as sialyl (α2,3) lactose and lacto-N-fucopentaose III, are reported to increase TLR signaling; under some circumstances this might contribute toward immunologic balance. Human milk on the whole is strongly anti-inflammatory, and contains abundant components that depress TLR signaling pathways: sTLR2 and sCD14 inhibit TLR2 signaling; sCD14, lactadherin, lactoferrin, and 2'-fucosyllactose attenuate TLR4 signaling; 3'-galactosyllactose inhibits TLR3 signaling, and β-defensin 2 inhibits TLR7 signaling. Feeding human milk to neonates decreases their risk of sepsis and necrotizing enterocolitis. Thus, the TLR regulatory components found in human milk hold promise as benign oral prophylactic and therapeutic treatments for the many gastrointestinal inflammatory disorders mediated by abnormal TLR signaling., (© 2016 American Society for Nutrition.)

The objective of the current study was to determine associations between the severity of systemic inflammation during the early postpartum period and performance, energy metabolism, and immune function in dairy cows. Cows were assigned to categorical quartiles (Q; Q1=0.18-0.59, Q2=0.60-1.14, Q3=1.15-2.05, and Q4=2.06-2.50 g of haptoglobin/L) based on the highest plasma haptoglobin (Hp) concentration measured during wk 1 postpartum. Although cows were assigned to different categories of inflammation during the postpartum period, we detected a quadratic relationship of inflammation on prepartum dry matter intake (DMI) and body weight (BW) such that cows in Q2 had lower prepartum DMI and cows in Q2 and Q3 had lower prepartum BW compared with cows in the other quartiles. We also detected a quadratic association of inflammation with postpartum DMI and BW such that cows in Q2 and Q3 also had generally lower postpartum DMI and BW compared with cows in Q1. There was a tendency for a Q × time interaction for milk yield and Q × time interactions for 3.5% fat-corrected milk and energy-corrected milk yields; quadratic relationships suggested decreased milk yield for Q2 and Q3 cows. We also found Q × parity and Q × time interactions for plasma glucose and insulin concentrations, suggesting alterations with differing degrees of inflammation. There was also a Q × time interaction for plasma nonesterified fatty acids concentration. In addition, alterations in liver triglyceride and glycogen contents for cows with inflammation as well as alterations in [1-(14)C]propionate oxidation in vitro were observed. Although we observed limited effects of inflammation on neutrophil and monocyte phagocytosis at d 7 postpartum, inflammation appeared to alter neutrophil and monocyte oxidative burst. Overall, cows with any degree of elevated haptoglobin in the first week after calving had alterations in both pre- and postpartum intake and postpartum metabolism., (Copyright © 2016 American Dairy Science Association. Published by Elsevier Inc. All rights reserved.)

The effect of circadian rhythm (CR) disruption on immune function depends on the method by which CRs are disrupted. Behavioral and thermoregulatory responses induced by lipopolysaccharide (LPS) treatment were assessed in female Siberian hamsters in which circadian locomotor activity (LMA) rhythms were eliminated by exposure to a disruptive phase-shifting protocol (DPS) that sustains arrhythmicity even when hamsters are housed in a light-dark cycle. This noninvasive treatment avoids genome manipulations and neurological damage associated with other models of CR disruption. Circadian rhythmic (RHYTH) and arrhythmic (ARR) hamsters housed in a 16L:8D photocycle were injected with bacterial LPS near the onset of the light (zeitgeber time 1; ZT1) or dark (ZT16) phase. LPS injections at ZT16 and ZT1 elicited febrile responses in both RHYTH and ARR hamsters, but the effect was attenuated in the arrhythmic females. In ZT16, LPS inhibited LMA in the dark phase immediately after injection but not on subsequent nights in both chronotypes; in contrast, LPS at ZT1 elicited more enduring (~4 day) locomotor hypoactivity in ARR than in RHYTH hamsters. Power and period of dark-phase ultradian rhythms (URs) in LMA and Tb were markedly altered by LPS treatment, as was the power in the circadian waveform. Disrupted circadian rhythms in this model system attenuated responses to LPS in a trait- and ZT-specific manner; changes in UR period and power are novel components of the acute-phase response to infection that may affect energy conservation., (© 2015 The Author(s).)

The objectives were to confirm that intravenous fish oil (FO) emulsions could alleviate acute lung injury, modulate immunity, and reduce inflammation in rats with abdominal sepsis and to explore the mechanisms of these effects. Thirty-six adult male Sprague-Dawley rats were divided into 4 groups randomly. Two days after central venous catheterization, rats were subjected to cecal ligation and puncture to produce abdominal sepsis. Rats were assigned to receive normal saline or total parenteral nutrition (TPN) containing standard soybean oil emulsions or FO-supplemented TPN at the onset of sepsis for 5 days. A sham operation and control treatment were performed in control group rats. Acute lung injury scores, peripheral blood lymphocyte subsets, plasma cytokines, and Foxp3 expression in the spleen were determined. Compared with the normal saline and TPN without FO, FO-supplemented TPN beneficially altered the distributions of the T-lymphocyte subsets and downregulated the acute lung injury scores, plasma cytokines, and expression of Foxp3 due to sepsis. Fish oil-supplemented TPN can decrease acute lung injury scores, alleviate histopathology, reduce the bacterial load in the peritoneal lavage fluid, modulate the lymphocyte subpopulation in the peripheral blood, downregulate Foxp3 expression in the spleen, and reduce plasma cytokines, which means that FO-supplemented TPN can alleviate acute lung injury, modulate immunity, and reduce inflammation in rats with abdominal sepsis., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Flavonoids, through a modulation of immune function, have been suggested to be involved in the role played by plant foods in disease prevention. We performed a systematic search in the MEDLINE database to review the effect of flavonoid-rich foods and flavonoids supplements on immune function. A total of 58 studies, were identified as suitable: 41 addressed in vivo proinflammatory cytokines and 15 measured ex vivo markers of immune function. According to our findings and on the basis of single food items, the number of studies in humans is limited and, for galenic supplements, only quercetin has been investigated. More evidences are needed to clarify the role of flavonoids as modulator of immune function in humans.

Sleep disorders have become a global issue, and discovering their causes and consequences are the focus of many research endeavors. An estimated 70 million Americans suffer from some form of sleep disorder. Certain sleep disorders have been shown to cause neurocognitive impairment such as decreased cognitive ability, slower response times and performance detriments. Recent research suggests that individuals with sleep abnormalities are also at greater risk of serious adverse health, economic consequences, and most importantly increased all-cause mortality. Several research studies support the associations among sleep, immune function and inflammation. Here, we review the current research linking sleep, immune function, and gastrointestinal diseases and discuss the interdependent relationship between sleep and these gastrointestinal disorders. Different physiologic processes including immune system and inflammatory cytokines help regulate the sleep. The inflammatory cytokines such as tumor necrosis factor, interleukin-1 (IL-1), and IL-6 have been shown to be a significant contributor of sleep disturbances. On the other hand, sleep disturbances such as sleep deprivation have been shown to up regulate these inflammatory cytokines. Alterations in these cytokine levels have been demonstrated in certain gastrointestinal diseases such as inflammatory bowel disease, gastro-esophageal reflux, liver disorders and colorectal cancer. In turn, abnormal sleep brought on by these diseases is shown to contribute to the severity of these same gastrointestinal diseases. Knowledge of these relationships will allow gastroenterologists a great opportunity to enhance the care of their patients.

Background: Patients undergoing hemodialysis (HD) have low plasma levels of zinc (Zn), high plasma levels of copper (Cu), and exhibit increased oxidative stress, inflammation, and immune abnormalities. We evaluated the effects of Zn supplementation on abnormal plasma Cu/Zn ratios and clinical outcomes in HD patients., Design and Methods: Patients on long-term HD with lower than normal plasma concentrations of Zn (< 80 mg/dL) were randomized to receive daily oral Zn supplements (n = 40) or no supplements (n = 25) for eight weeks. Age- and sex-matched healthy individuals served as a control group (n = 38). A number of clinical parameters were measured before and after the supplementation period., Results: Compared with healthy subjects, patients had significantly elevated plasma Cu concentrations and Cu/Zn ratios, as well as higher levels of oxidative stress and pro-inflammatory cytokines. Patients who received Zn supplements for eight weeks had higher plasma concentrations of Zn and lower concentrations of Cu, along with reduced Cu/Zn ratios, oxidative stress status, and inflammatory responses compared to patients who did not receive Zn. Patients receiving Zn also showed significantly higher percentages of CD4 and CD19 lymphocytes, and elevated CD4/CD8 ratios., Conclusions: Zn supplementation ameliorates abnormally high plasma Cu/Zn ratios and may reduce oxidative stress, improve inflammatory status, and maintain immune function in patients undergoing long-term HD.

Postoperative bacterial infections are common despite prophylactic administration of antibiotics. The wide-spread use of antibiotics in patients has contributed to the emergence of multiresistant bacteria. A restricted use of antibiotics must be followed in most clinical situations. In surgical patients there are several reasons for an altered microbial flora in the gut in combination with an altered barrier function leading to an enhanced inflammatory response to surgery. Several experimental and clinical studies have shown that probiotics (mainly lactobacilli) may reduce the number of potentially pathogenia bacteria (PPM) and restore a deranged barrier function. It is therefore of interest to test if these abilities of probiotics can be utilized in preoperative prophylaxis. These factors may be corrected by perioperative administration of probiotics in addition to antibiotics. Fourteen randomized clinical trials have been presented in which the effect of such regimens has been tested. It seems that in patients undergoing liver transplantation or elective surgery in the upper gastrointestinal tract prophylactic administration of different probiotic strains in combination with different fibers results in a three-fold reduction in postoperative infections. In parallel there seems to be a reduction in postoperative inflammation, although that has not been studied in a systematic way. The use of similar concepts in colorectal surgery has not been successful in reducing postoperative infections. Reasons for this difference are not obvious. It may be that higher doses of probiotics with longer duration are needed to influence microbiota in the lower gastrointestinal tract or that immune function in colorectal patients may not be as important as in transplantation or surgery in the upper gastrointestinal tract. The favorable results for the use of prophylactic probiotics in some settings warrant further controlled studies to elucidate potential mechanisms, impact on gut microbiota and influence on clinical management. The use of probiotics must be better delineated in relation to type of bacteria, dose and length of administration.

Background: Traffic-related air pollution has been associated with adverse health outcomes, and the immune system may be a biologic mediator of health effects., Objectives: We analyzed associations between living near major roads and immune status as measured by five immune assays. We hypothesized that living near a freeway, arterial, or truck route would be associated with increased inflammation and decreased immune function., Methods: We used a geographic information system (GIS) to determine residential proximity to major roads among 115 postmenopausal, overweight women in the greater Seattle, Washington (USA), area whose immunity was assessed at the baseline visit of an exercise intervention trial. We evaluated three inflammatory markers (C-reactive protein, serum amyloid A, and interleukin-6) and two functional assays of cellular immunity [natural killer (NK) cell cytotoxicity and T-lymphocyte proliferation]., Results: Women living within 150 m of arterial roads had 21% lower NK cytotoxicity compared with women who lived farther from an arterial [mean cytotoxicity, 19.5%; 95% confidence interval (CI), 15.6-23.5%; vs. mean cytotoxicity, 24.8%; 95% CI, 22.0-27.5%], after adjustment for both individual-level and census tract-level demographic characteristics. This association was limited to women who reported exercising near traffic. Fewer women lived near freeways and truck routes. Markers of inflammation and lymphocyte proliferation did not consistently differ according to proximity to major roads., Conclusions: If the observed association between residential proximity to traffic and decreased NK cytotoxicity is confirmed in other populations, our results may have implications for local land use policy.

Introduction: Sleep quality is increasingly acknowledged as critical for immune function and overall health. Poor sleep can disrupt immune response, elevating inflammation and susceptibility to infection and chronic diseases. Given the prevalence of sleep disturbances across populations, understanding their impact on immune health and overall wellness is essential. Purpose of Work: This review aims to examine the relationship between sleep quality and immune function by synthesizing findings on how poor sleep contributes to immune suppression, heightened inflammation, and mental health disturbances, particularly in vulnerable populations. This review also explores possible interventions to mitigate these effects. Material and Methods: A literature search was conducted on databases including PubMed and Google Scholar, focusing on studies from 2012 to 2023. Articles assessing sleep quality, immune markers, and the mediating roles of stress and depression were reviewed. Criteria included studies with both subjective and objective assessments of sleep, immune function, and relevant mental health markers. Summary: Findings indicate that poor sleep quality negatively impacts immune health, primarily through increased systemic inflammation and decreased immune cell functionality. Depression and stress further exacerbate these effects, particularly in populations with chronic illnesses or high psychological distress. Targeted interventions that improve sleep quality and manage stress may bolster immune resilience and overall health. Future research should continue to address these interactions across diverse populations to develop targeted interventions. [ABSTRACT FROM AUTHOR]

Objective: To investigate effect of trimetazidine (TMZ) on immune function of Streptococcus pneumoniae (SP) pneumonia rats through cyclic guanylate adenylate synthase (cGAS)-stimulator of interferon gene (STING) pathway. Methods: Rats were randomly separated into model group, TMZ group and DMXAA group (cGAS-STING signaling pathway activator). SP pneumonia rat model was replicated by intranasal instillation of SP, while rats in control group were infused with an equal amount of physiological saline. ELISA was applied to detect IL-1β and IL-10 levels. Flow cytometry was applied to detect CD4*T and CD8*T levels. Spleen and thymus indexes of rats in each group were compared. Transmission turbidity method was applied to detect IgG and IgA levels. HE staining was applied to observe pathological changes in lung tissue. Western blot was applied to detect cGAS-STING pathway proteins expressions. Results: Compared with control group, rats in model group showed an increase in alveolar wall and lung interstitium, accompanied by edema, bleeding and inflammatory cell infiltration, IL-1β, CD8*T cells levels, lung tissue pathological injury score, cGAS, STING expressions were increased, IL-10, CD4*T cells levels, CD4*T/CD8*T, spleen and thymus indexes, IgG, IgA levels were decreased (P<0.05). Compared with model group, rats in TMZ group showed reduced thickening of alveolar walls, great improvement in alveolar structure, and less infiltration of inflammatory cells, IL-1β, CD8*T cells levels, lung tissue pathological injury score, cGAS, STING expressions were decreased, IL-10, CD4*T cells levels, CD4*T/CD8*T, spleen and thymus indexes, IgG, IgA levels were increased (P<0.05). Compared with TMZ group, IL-1(3, CD8*T levels, pathological injury score of lung tissue, cGAS and STING expressions in DMXAA group were increased, while IL-10, CD4*T cells levels, CD4*T/CD8*T, spleen and thymus index, IgG and IgA levels were decreased (P<0.05). Conclusion: TMZ may inhibit inflammation by inhibiting cGAS-STING signaling pathway, and enhance immune function of rats with SP pneumonia. [ABSTRACT FROM AUTHOR]

Introduction Sleep quality is increasingly acknowledged as critical for immune function and overall health. Poor sleep can disrupt immune response, elevating inflammation and susceptibility to infection and chronic diseases. Given the prevalence of sleep disturbances across populations, understanding their impact on immune health and overall wellness is essential. Purpose of Work This review aims to examine the relationship between sleep quality and immune function by synthesizing findings on how poor sleep contributes to immune suppression, heightened inflammation, and mental health disturbances, particularly in vulnerable populations. This review also explores possible interventions to mitigate these effects. Material and Methods A literature search was conducted on databases including PubMed and Google Scholar, focusing on studies from 2012 to 2023. Articles assessing sleep quality, immune markers, and the mediating roles of stress and depression were reviewed. Criteria included studies with both subjective and objective assessments of sleep, immune function, and relevant mental health markers. Summary Findings indicate that poor sleep quality negatively impacts immune health, primarily through increased systemic inflammation and decreased immune cell functionality. Depression and stress further exacerbate these effects, particularly in populations with chronic illnesses or high psychological distress. Targeted interventions that improve sleep quality and manage stress may bolster immune resilience and overall health. Future research should continue to address these interactions across diverse populations to develop targeted interventions.

ObjectiveChronic stress adversely affects cognition, in part due to stress-induced inflammation. Rodent models suggest females are more resilient against stress-related cognitive dysfunction than males; however, few studies have examined this in humans. We examined sex differences in the relationship between perceived stress, cognitive functioning, and peripheral inflammation over time among cognitively normal older adults.DesignLongitudinal observational study.SettingUniversity research center.Participants274 community-dwelling older adults (baseline age: M=70.7, SD=7.2; 58% women; Clinical Dementia Rating=0) who completed at least two study visits.MeasurementsNeurocognitive functioning and perceived stress (Perceived Stress Scale [PSS]) were assessed at each visit. Plasma was analyzed for interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) in a subset of 147 participants. Linear mixed effects models examined the interaction between average PSS (i.e., averaged within persons across visits), sex, and time on cognitive domains and on inflammatory markers.ResultsThe interaction between stress, sex, and time predicted executive functioning (β = 0.26, SE = 0.10, p = 0.01) such that higher average PSS related to steeper declines in men, but not in women. Among the 147 participants with inflammatory data, higher average PSS was associated with steeper increases in IL-6 over time in men, but not in women.ConclusionConsistent with animal models, results showed older men were more vulnerable to negative effects of stress on cognitive aging, with domain-specific declines in executive function. Findings also suggest systemic immunological mechanisms may underlie increased risk for cognitive decline in men with higher levels of stress. Future work is needed to examine the potential efficacy of person-specific stress interventions.

Background. Exercise-induced muscle damage (EIMD) is a temporary response to intense or prolonged exercise that can cause muscle pain, inflammation, and impaired muscle function. Antioxidant supplementation is a proposed strategy to reduce EIMD symptoms by targeting reactive oxygen and nitrogen species (RONS) involved in the process. Objective. The study aimed to investigate the effect of Selenomethionine supplementation on malondialdehyde (MDA) and C-reactive protein (CRP) levels resulting from Exercise-Induced Muscle Damage (EIMD). Materials and methods. This study used a randomized pretest-posttest control group design, involving a total of 32 male recreational students from the State University of Surabaya (Indonesian: Universitas Negeri Surabaya), (age 19.25 ± 0.76 years, body mass 63.16 ± 3.38 kg, height 167.28 ± 4.54 cm, body fat 19.60% ± 4.57%). The participants were randomly assigned to the selenomethionine group (SEM, 100 µg/day) or placebo group (PLA, corn starch 100 mg/day) for a period of 28 days (4 weeks). On days 1 (baseline) and 29, participants underwent a single bout of EIMD. Blood samples were collected 24 hours post-EIMD to measure MDA and CRP concentrations in plasma. The statistical analysis was conducted using paired sample t-test. Results. The placebo group experienced a significant increase in plasma MDA and CRP concentrations after EIMD compared with baseline values (p < 0.05). However, the SeMet group showed lower plasma MDA and CRP levels than the placebo group. Conclusions. Daily Selenomethionine supplementation for 28 days has been found to reduce oxidative stress by lowering MDA levels in the blood and to decrease inflammation by reducing CRP levels post-exercise-induced muscle damage. This indicates a lower risk of EIMD due to reduced oxidative stress and inflammation.

Summary: Sickle cell anaemia (SCA) patients display elevated levels of circulating pro‐inflammatory cytokines and endothelial activation markers compared to healthy peers. The impact of exercise on the pro‐inflammatory state in SCA remains unclear. This study aimed to characterize the whole‐blood transcriptome profile in response to an acute bout of exercise in paediatric SCA patients. Twenty‐three SCA participants (13 ± 3 years, 52% girls) and 17 healthy controls (14 ± 3 years, 29% girls) performed eight 2‐min bouts of cycle ergometry interspersed with 1‐min rest intervals. Whole‐blood transcriptome profile (RNA‐seq) was performed before and after exercise. At baseline, gene pathways associated with gas transport in erythrocytes were up‐regulated in SCA patients compared to controls. Following exercise, gene pathways associated with innate immunity were altered in both groups. Interaction analyses revealed 160 annotated genes (101 up‐ and 59 down‐regulated) that differentially altered by exercise in SCA patients. Moreover, genes that exhibited a blunted response to exercise in SCA patients were enriched in the IL‐17 signalling pathway, suggesting an impaired innate immune response to exercise. This data will contribute to the development of evidence‐based exercise prescription guidelines for this patient population. [ABSTRACT FROM AUTHOR]

Background. Exercise-induced muscle damage (EIMD) is a temporary response to intense or prolonged exercise that can cause muscle pain, inflammation, and impaired muscle function. Antioxidant supplementation is a proposed strategy to reduce EIMD symptoms by targeting reactive oxygen and nitrogen species (RONS) involved in the process. Objective. The study aimed to investigate the effect of Selenomethionine supplementation on malondialdehyde (MDA) and C-reactive protein (CRP) levels resulting from Exercise-Induced Muscle Damage (EIMD). Materials and methods. This study used a randomized pretest-posttest control group design, involving a total of 32 male recreational students from the Universitas Negeri Surabaya, (age 19.25 ± 0.76 years, body mass 63.16 ± 3.38 kg, height 167.28 ± 4.54 cm, body fat 19.60% ± 4.57%). The participants were randomly assigned to the selenomethionine group (SEM, 100 μg/day) or placebo group (PLA, corn starch 100 mg/day) for a period of 28 days (4 weeks). On days 1 (baseline) and 29, participants underwent a single bout of EIMD. Blood samples were collected 24 hours post-EIMD to measure MDA and CRP concentrations in plasma. The statistical analysis was conducted using paired sample t-test. Results. The placebo group experienced a significant increase in plasma MDA and CRP concentrations after EIMD compared with baseline values (p < 0.05). However, the SeMet group showed lower plasma MDA and CRP levels than the placebo group. Conclusions. Daily Selenomethionine supplementation for 28 days has been found to reduce oxidative stress by lowering MDA levels in the blood and to decrease inflammation by reducing CRP levels post-exercise-induced muscle damage. This indicates a lower risk of EIMD due to reduced oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

This study investigated the effects of Periplaneta americana residue (PAR) on the immune function, antioxidant capacity, and transcriptome of Sanhuang chickens. Six hundred 30-day-old Sanhuang chickens were divided into six groups with diets of varying PAR replacement of soybean meal from 0 to 100% in increments of 20%. Samples were taken on day 100. The results indicated that PAR did not significantly affect growth performance (p > 0.05). PAR significantly elevated the levels of IL-1β, IL-2, TNF-α, IgA, IgG, and IgM in both the serum and spleen (p < 0.05). Moreover, it markedly increased the GSH-Px, T-AOC, SOD, and CAT levels in the serum and liver (p < 0.05) and reached optimal levels of immune factors and antioxidant indicators at diet 2. Transcriptomic analysis revealed that substituting PAR for soybean meal downregulated genes associated with immune diseases and infectious disease pathways. Substituting soybean meal with PAR enhanced the resistance of Sanhuang chickens to pathogenic factors and oxidative stress, with no impact on growth performance. The optimal improvement was observed with diet 2.

Introduction: Ambient air pollution is a neurotoxicant with hypothesized immune-related mechanisms. Adolescent brain structural and functional connectivity may be especially vulnerable to ambient pollution due to the refinement of large-scale brain networks during this period, which vary by sex and have important implications for cognitive, behavioral, and emotional functioning. In the current study we explored associations between air pollutants, immune markers, and structural and functional connectivity in early adolescence by leveraging cross-sectional sex-stratified data from the Adolescent Brain Cognitive Development℠ Study®. Methods: Pollutant concentrations of fine particulate matter, nitrogen dioxide, and ozone were assigned to each child's primary residential address during the prenatal period and childhood (9-10 years-old) using an ensemble-based modeling approach. Data collected at 11-13 years-old included resting-state functional connectivity of the default mode, frontoparietal, and salience networks and limbic regions of interest, intracellular directional and isotropic diffusion of available white matter tracts, and markers of cellular immune activation. Using partial least squares correlation, a multivariate data-driven method that identifies important variables within latent dimensions, we investigated associations between 1) pollutants and structural and functional connectivity, 2) pollutants and immune markers, and 3) immune markers and structural and functional connectivity, in each sex separately. Results: Air pollution exposure was related to white matter intracellular directional and isotropic diffusion at ages 11–13 years, but the direction of associations varied by sex. There were no associations between pollutants and resting-state functional connectivity at ages 11–13 years. Childhood exposure to nitrogen dioxide was negatively correlated with white blood cell count in males. Immune biomarkers were positively correlated with white matter intracellular directional diffusion in females and both white matter intracellular directional and isotropic diffusion in males. Lastly, there was a reliable negative correlation between lymphocyte-to-monocyte ratio and default mode network resting-state functional connectivity in females, as well as a compromised immune marker profile associated with lower resting-state functional connectivity between the salience network and the left hippocampus in males. In post-hoc exploratory analyses, we found that the PLSC-identified white matter tracts and resting-state networks related to processing speed and cognitive control performance from the NIH Toolbox. Conclusions: We identified novel links between childhood nitrogen dioxide and cellular immune activation in males, and brain network connectivity and immune markers in both sexes. Future research should explore the potentially mediating role of immune activity in how pollutants affect neurological outcomes as well as the potential consequences of immune-related patterns of brain connectivity in service of improved brain health for all.

Although seasonal changes in physiology are well documented, little is known about how human immune and metabolic markers vary across seasons, and no studies have examined how stress → health biomarker associations differ across the year. To investigate these issues, we analyzed data from 2118 participants of the Midlife in the United States (MIDUS) study to determine whether there were differences in (a) levels of 19 immune and metabolic markers, and (b) the association between perceived stress and each biomarker across the year. Results of component-wide boosted generalized additive models revealed seasonal patterning for most biomarkers, with immune proteins generally peaking when days were shorter. Moreover, whereas levels of hemoglobin A1C rose from late fall to spring, triglycerides were elevated in the summer and fall, and high-density lipoprotein decreased steadily from January to December. Urinary cortisol and cortisone exhibited opposite patterns, peaking at the beginning and end of the year, respectively. Most critically, we found that the effects of perceived stress on 18 of the 19 health biomarkers assessed varied by month of measurement. In some cases, these differences involved the magnitude of the stress → biomarker association but, in other cases, it was the direction of the effect that changed. Studies that do not account for month of biomarker assessment may thus yield misleading or unreproducible results.