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Background: Host genetic factors can influence susceptibility, morbidity and mortality from schistosomiasis. The study explored the association between single nucleotide polymorphisms (SNPs) in interleukin-10 (IL-10) and tumour necrosis factor alpha (TNF-a) promoter regions and susceptibility to Schistosoma haematobium infection. Methods: Urine specimens were collected from 361 primary school children aged 5-15 years from schistosomiasis endemic areas of Manicaland and Mashonaland central provinces. Schistosoma haematobium was diagnosed using the urine filtration method. Only 272 participants provided adequate blood for genotyping. Genotyping was performed using the amplification refractory mutation system-polymerase chain reaction. The association between IL-10 and TNF-a SNPs and S. haematobium infection was analysed using the chi-square test. Results: Schistosoma haematobium infection was confirmed in 26.8% of the participants. No significant difference in S. haematobium prevalence between men (51.6% of those infected) and women (48.4%) (X² = 0.008, df = 1, p = 0.928) was observed. The total IL-10 -1082 G, IL-10 -819 C and TNF-a -308G allele distribution between S. haematobium infected and uninfected participants was 50.7% and 51.5% (X² = 0.025, df = 1, p = 0.87), 54.3% and 60.6% (X² = 1.187, df = 1, p = 0.187) and 82.1% and 80.9% (X² = 0.099, df = 1, p = 0.753), respectively, and the differences were not significant. Conclusion: Interleukin-10 -1082 G/A, IL-10 -819 C/T and TNF-a -308 G/A SNPs were not significantly associated with susceptibility to S. haematobium infection. The prevalence of schistosomiasis is still in the moderate range and is similar in boys and girls. [ABSTRACT FROM AUTHOR]

Background/Aim: The aim of this study was to evaluate whether the altered profile of adipocytokine and genetic fingerprint in NAFLD-associated metabolic syndrome "cluster" represents synergistic risk factors predicting onset of liver colorectal cancer metastases. Materials and Methods: A total of 165 colorectal cancer patients were enrolled, 56,3% were with metabolic syndrome/NAFLD. Serum samples were assayed for ADIPOQ, leptin and TNF-a levels by ELISA. ADIPOQ rs266729 C/G and TNF-308 A/G genotypes were analyzed in DNA isolated from whole blood. Results: Reduction in adiponectin levels and increase in leptin and TNF-a was shown in patients with liver metastases. This trend was influenced by BMI, MetS/NAFLD, and insulin resistance. ADIPOQ G rs266729 and TNF- 308 A allele are associated with obesity, MetS/NAFLD and insulin resistance. ADIPOQ CG/GG and GA/AA TNF-alpha genotypes confer susceptibility to liver metastases. Conclusion: Obesity and hepatic steatosis significantly favor the development of colorectal cancer liver metastases and the individual adipocytokines genetic profile may play an important predictive role. [ABSTRACT FROM AUTHOR]

Silymarin (SL), a flavonolignan complex isolated from seeds of Silybum marianum (Asteraceae), is known for its hepatoprotective, anti-apoptotic, anti-inflammatory, and antioxidant activities. A glycopeptide antibiotic, Vancomycin (VA) which is used for the treatment of serious infections caused by multi-resistant Gram-positive microorganisms has been clinically used for a long time. The aim of the present study was to evaluate potential therapeutic efficiency of SL against VA-induced apoptosis and inflammation using apoptotic (caspase-3, -8, and, -9 enzyme activities) and inflammatory (Tumor necrosis factor-alpha (TNF-a)) markers, and histopathological examinations in rat liver. A total of 49 male Wistar albino rats was divided into 7 groups including control (saline, intraperitoneally (i.p.)), Dimethyl sulfoxide (i.p.), VA (400 mg/kg/day, i.p.), SL100 (100 mg/kg/day, i.p.), VA+SL50 (50 mg/kg/day, i.p.), VA+SL100 (100 mg/kg/day, i.p.), and VA+SL200 (200 mg/kg/day, i.p.). SL was administered once a daily for 8 days. One day after the first treatment of SL, VA administration was started and continued for 7 days. Hepatic TNF-a levels were evaluated by ELISA and hepatic caspase activities were evaluated according to the colorimetric method. Significantly increased caspase activities were determined in VA group compared to control group (P<0.05). However, significantly reduced caspase activities were determined in VA+SL200 group when compared to VA group (P<0.05). TNF-a level in VA group was found to be statistically higher than control group (P<0.05). TNF-a levels of SL100, VA+SL (50, 100, and 200) groups were significantly lower than VA group (P<0.05). VA+SL200 group was found to be the most effective group according to reducing caspase activities and TNF-a level. [ABSTRACT FROM AUTHOR]

Post-traumatic mortality rates are still very high and show an increasing tendency. Early identification of patients at high risk of severe complications has a significant impact on treatment outcomes. The aim of the study was to better understand the early pathological inflammatory response to injury and infection, and to determine the usefulness of the assessment of TNF-a and sTNFR1 concentrations in the peripheral blood as early indicators of severe post-traumatic complications. The study was carried out in a group of 51 patients after trauma, treated in the ED, including 32 patients who met the inclusion criteria for immunological analysis. Patients were divided into two groups using the ISS scale (A ISS = 20, B ISS < 20). The highest TNF-a and sTNFR1 concentrations in both groups were recorded at admission and were significantly higher in group A compared to group B (A vs. B TNF-a 2.46 pg/ml vs. 1.78 pg/ml; sTNFR1 1667.5 pg/ml vs. 875.2 p < 0.005). The concentration of sTNFR1 in patients with severe complications was significantly higher compared to patients without complications and preceded clinical symptoms of complications (C+ vs. C- 1561.5 pg/ml vs. 930.6 pg/ml, p < 0,005). The high diagnostic sensitivity calculated from the ROC curves was found for the concentrations of both cytokines: TNF-a (AUC = 0.91, p = 0.004) and sTNFR1 (AUC = 0.86, p = 0.011). Elevated levels of sTNFR1, determined in the peripheral blood shortly after injury, are significantly associated with the occurrence of later complications, which in some patients lead to death. In contrast, high levels of TNF-a shortly after injury are associated with mortality. [ABSTRACT FROM AUTHOR]

Background: Probiotic use to prevent gastrointestinal infections in critical care has shown great promise in recent clinical trials. Although well-documented benefits of probiotic use in intestinal disorders, the potential for probiotic treatment to ameliorate liver injury and hypoxic hepatitis following sepsis has not been well explored.Methods: In order to evaluate, if Lactobacillus rhamnosus GG (LGG) treatment in septic rats will protect against liver injury, this study used 20-22-week-old Sprague-Dawley rats which were subjected to cecal ligation and puncture to establish sepsis model and examine mRNA and protein levels of IL-1β, NLRP3, IL-6, TNF-a, VEGF, MCP1, NF-kB and HIF-1α in the liver via real-time PCR, Elisa and Western blot.Results: This study showed that LGG treatment significantly ameliorated liver injury following experimental infection and sepsis. Liver mRNA and protein levels of IL-1β, NLRP3, IL-6, TNF-a, VEGF, MCP1, NF-kB and HIF-1α were significantly reduced in rats receiving LGG.Conclusions: Thus, our study demonstrated that LGG treatment can reduce liver injury following experimental infection and sepsis and is associated with improved hypoxic hepatitis. Probiotic therapy may be a promising intervention to ameliorate clinical liver injury and hypoxic hepatitis following systemic infection and sepsis. [ABSTRACT FROM AUTHOR]

Background: In Iraq, a high prevalence rate of Toxoplasma gondii infection was reported and data about correlation between this infection and major depressive disorders were documented. Therefore, the aim of current study was to evaluate the association between levels of parameters related to chronic toxoplasmosis infection and depression in Iraq women. Method: In this study, 260 serum samples were collected from Iraqi women and divided into four groups as follow: G1 depressed women infected with toxoplasmosis, G2 women infected with toxoplasmosis but did not have depression, G3 depressed women without toxoplasmosis infection with toxoplasmosis, G4 apparently healthy persons. The following parameters were assessed TNF-a, IL-17, IL-33, TGF-b and dopamine. Statistical analysis was performed by using statistical analysis system. Results: Data from current study revealed elevated levels of proinflammatory cytokines TNF-a, IL-33, IL- 17, as well as there was an increase in concentration of dopamine in G1. The mean ± SE levels for the three cytokines were (2444.69 ± 98.82, 3629.50 ± 61.10 and 1008.88 ± 36.35 pg/ml), respectively and the mean ± SE for dopamine was (387.33 ± 8.09 pg/ml), while TGF-b didn't show any elevation in its level in this group. Conclusion: Elevated levels of both proinflammatory cytokines and dopamine in depressed women who had chronic infection of toxoplasmosis may reflect the effect of chronic infection that may alter the expression of dopamine which skew the immune response towered Th17 that affect the expression level of proinflammatory cytokines and neutrophils response. [ABSTRACT FROM AUTHOR]

Bone homeostasis is preserved by the balance of maintaining between the activity of osteogenesis and osteoclastogenesis. However, investigations for the osteoclastogenesis were hampered by considerable difficulties associated with isolating and culturing osteoclast in vivo. As the alternative, stimuli‐induced osteoclasts formation from RAW264.7 cells (RAW‐OCs) have gain its importance for extensively osteoclastogenic study of bone diseases, such as rheumatoid arthritis, osteoporosis, osteolysis and periodontitis. However, considering the RAW‐OCs have not yet been well‐characterized and RAW264.7 cells are polymorphic because of a diverse phenotype of the individual cells comprising this cell linage, and different fate associated with various stimuli contributions. Thus, in present study, we provide an overview for current knowledge of the phenotype of RAW264.7 cells, as well as the current understanding of the complicated interactions between various stimuli and RAW‐OCs in the light of the recent progress. [ABSTRACT FROM AUTHOR]

Introduction: The massive implementation of combination antiretroviral therapy (cART) has forever changed the landscape of HIV infection. This unprecedented success has turned HIV infection into a manageable chronic disease. The increased survival of people living with HIV is, however, shadowed by a high burden of aging-related comorbidities. The pathogenic basis underlying this excess of co-morbid conditions is most likely a persistent inflammatory and immune activation state, despite an optimal control of HIV replication, which in turn has largely been attributed to bacterial or bacterial products translocation from the gut. Area covered: This review is focused on the relationship between cART and the chronic inflammatory and immune activation status in otherwise virologically well-controlled people living with HIV (PLWH). Particular focus will be placed on the differences, if any, between distinct cART modalities, with emphasis on less-drug cART regimens, and especially on dual therapies. Expert opinion: Research to address the increased inflammatory and immune activation status of cART-treated, HIV-infected patients, should focus on adjuvant means of therapy, rather than on the cART regime itself. With current antiretrovirals, no difference between dual and triple regimens has been demonstrated, provided that virological and immunological outcomes be non-inferior. [ABSTRACT FROM AUTHOR]

Background: Cystic ovarian disease (COD) is one of the common reproductive disorders which affecting the fertility of dairy cattle induces heavy financial burdens on herds owners. Various insecticides, fungicides and herbicides, collectively known as pesticides are frequently used in the agricultural systems of different countries. Given the fact that pesticides are known to have endocrine disrupting properties, exposure to these compounds may play a role in the development of COD. Materials and Methods: The plasma concentrations of a complete profile of common pesticides including organophosphorus, organochlorine, and carbamate and pyrethroid compounds in the plasma of cattle with COD compared to healthy controls was examined. Moreover, plasma concentrations of inflammatory cytokines as well as oxidative stress parameters were investigated. Results: No significant amounts of any of the pesticides investigated were detectable in the plasma of neither the healthy nor cystic cows. The plasma indices of total antioxidant capacity (TAC), thiol, lipid peroxidation (LPO), and reactive oxygen species (ROS) did not show any significant differences between the affected and the control groups. Tumor necrosis factors alpha (TNF-α), progesterone, lymphocyte, neutrophil, fibrinogen and MCHC had significantly higher amounts in the plasma of COD cows. Conclusion: Findings of the present study do not support the notion that exposure to the studied pesticides is a contributing factor in the development of follicular cysts in dairy cattle. In addition, TNF-α might be affected as a factor in the pathogenesis of COD by an independent pathway of pesticides effect. [ABSTRACT FROM AUTHOR]

Lower respiratory tract disease (LRT) a major public health problems with high mortality and one of the common causes of morbidity in children. Cytokines play a key role in the inflammatory process and pathogenesis of LRT disease. So the study aimed to detection the association between imbalance in pro- and anti-inflammatory biomarkers as cytokines (IL-6, TNF-á and IL-10) level and the development or progress some LRT disease such as bronchiolitis, bronchopneumonia and bronchial asthma. Case-control hospital study was performed of 100 patients with LRT disease in Baghdad Teaching Hospital in Baghdad city, Iraq with group of 30 healthy individual was used as control, the patients were divided according to types of disease into bronchiolitis 40 patients; bronchial asthma 38 patients and 22 patients suffering from pneumonia. The results revealed that percentage of male : female in both bronchiolitis and pneumonia was no significant different while the female were more than male in asthma and younger children more infected than aged children in LRT disease. The pro-inflammatory cytokine were increased in all diseases with higher level recorded in asthma then in bronchiolitis finally in pneumonia. In other hand the antiinflammatory cytokine appear that the asthma revealed high decreased then the bronchiolitis, finally the pneumonia. In conclusion, the imbalance in pro-inflammatory cytokine with increased their serum levels ,vs decreased the serum level of anti-inflammatory lead to persistence the inflammatory response and severity of respiratory disease. Also, the defect in cytokines level lead to increase the progression of LRT disease and can be consider as risk factor. [ABSTRACT FROM AUTHOR]

The etiology of lung cancer (LC) is a multifactorial and reflects the interaction between environment and genetic factors. Single nucleotide polymorphism (SNPs) in the promoter region of some cytokines may affect the overall expression of the cytokine, and, hence, involve in the development of cancer. This study aimed to evaluate the association of two SNPs in the promoter region of TNF-á gene and serum of TNF-á level of in the development of LC. A total of 50 patients with LC and other age-matched 40 apparently healthy individuals were enrolled in this casecontrol study. From each participant, 5 mL of peripheral blood were collected. DNA was isolated from leukocytes and TNF-á gene was amplified with two specific sets of primers. Genotyping was achieved by restriction fragment length polymorphism (RFLP). Serum level of TNF-á was measured using enzyme linked immune-sorbent assay (ELISA). The frequency of GG, GA and AA genotypes of the SNPTNF-á-308G/A among patients was 38%, 44% and 18%, respectively compared with 60%, 37.5% and 2.5% respectively among controls. Logistic regression test revealed a significant difference in the frequency of variant genotype (AA) between the two groups (OR=11.37, 95%CI = 1.32-97.78, P=0.027). The variant allele (A allele) of this polymorphism almost 2-time more frequent in patients than controls with a significant difference (OR=2.47,95%CI=1.27-4.82, P=0.012). No significant differences in the frequencies of genotypes and allele of TNF-á-863C/A between patients and controls. serum level of TNF-á in patients was 15 pg/mL (range 0-84 pg/mL) which is higher than that of controls (median 7 pg/mL, range 0-86 pg/mL) with a significant difference (P=0.022). These data suggest the importance of TNF-á-308G/A gene polymorphism as a risk factor for LC. Serum levels of TNFá increased in patients with active LC. [ABSTRACT FROM AUTHOR]

Multiple mechanisms and over 100 known physiologic intrinsic factors contribute to wound healing deficiencies in individuals with diabetic foot ulcer. Cross-sectional study was conducted on two groups of Iraqi patients with type-2 diabetes mellitus, the first group include 61 patients suffering from diabetic foot ulcer (DFU+), while the second group include 20 patients without diabetic ulcer (DFU-) that act as control. Based on Wagner classification system, the grade of foot ulcer was identified. Two samples (blood and saliva) were obtained from all patients at morning. The concentrations VEGF and TNF-á were determined in serum and saliva samples for all patients. The results showed non-significant difference in the serum level of VEGF between DM patients of DFU- and DFU+ groups, but its level in the saliva is significantly elevated in DFU+ group compared with DFU- group. In contrast to VEGF, the level of TNF-á in both samples (blood and saliva) is significantly elevated in DM patients of DFU+ group. Furthermore, the salivary index (SI) (i.e. ratio of biomarker concentration between saliva and blood for each patient) of VEGF in DM patients of DFU+ group is significantly higher than (SI) of those in DFU- group. Similarly, the calculated salivary index (SI) of TNF-á is significantly elevated in DM patients of DFU+ group when compared with that of DM patients in DFU- group. On the other hand, the correlation of VEGF level in the blood and saliva of patients with diabetic foot ulcer revealed non-significant association with grade of DFU, however, significant positive correlation was recorded between the grade of DFU and the TNF-á level in blood and saliva. It can be concluded that both biomarkers (VEGF, and TNF-á) are detectable in the saliva sample of DFU patients and saliva can serve as a good alternative sample than blood for the detecting of these biomarkers. However, only TNF-á appears as a promising markers to predict the risk of DFU development in DM patients and the severity of ulceration as well. [ABSTRACT FROM AUTHOR]

To determine the relationship between infertility and Helicobacter pylori infection, thirty-five infertile patients of ages (20-49) years have been investigated and compared with 10 apparently firtility individuals. All the studied groups were carried out to measure (ASA), (TNF-á), (IL-6), (anti-H.pylori IgA) and (anti-H.pyloriIgG) by Enzyme linked immunosorbent assay (ELISA) technique. The statistical analysis also demonstrated that there were a highly significant differences (P<0.01), when compared between studied group. Also, the statistical analysis demonstrated that there were a highly significant differences (P<0.01) when compare between infertility and fertility in Conc. of sperm. The percentage distribution of ASA in serum and semen was 8.57%, TNF-á was 11.43% in serumand there were a highly significant differences (P<0.01), the percentage distribution of IL-6 was 8.57% in serum and anti- H.pylori IgA was 57.14% in serum while, anti-H.pylori IgG was 100% in serum and 25.71% in semenand there were a highly significant differences (P<0.01). In conclusion, we propose that infection with H. pylori play an important role in male infertility. [ABSTRACT FROM AUTHOR]

João P Barbosa,1–3,* Ana R Neves,3,* Andreia M Silva,1,2,4 Mário A Barbosa,1,2,4 M Salette Reis,3 Susana G Santos1,2 1Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Portugal; 2INEB - Instituto de Engenharia Biomédica, Universidade do Porto, Portugal; 3UCIBIO, REQUIMTE, Chemical Sciences Department, Faculty of Pharmacy, University of Porto, Portugal; 4Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal *These authors contributed equally to this work Abstract: Dendritic cells (DCs) are promising targets for drug delivery, as they can induce immunity or tolerance. The current study aims to examine the potential of using nanostructured lipid carriers (NLC) as delivery systems for human DC by evaluating nanoparticle internalization, cell labeling, and drug activity. NLC were formulated incorporating the fluorochrome fluorescein isothiocyanate (FITC-NLC) or the natural anti-inflammatory molecule resveratrol (rsv-NLC). Primary human DCs were differentiated from peripheral blood monocytes, and the innovative imaging flow cytometry technique was used to examine FITC-NLC internalization. The capacity of rsv-NLC to inhibit DC activation in response to proinflammatory cytokine tumor necrosis factor-α (TNF-α) was investigated by conventional flow cytometry. A combination of imaging and conventional flow cytometry was used to assess NLC cytotoxicity. The results obtained indicate that both NLC formulations were stable over time, with mean diameter

Aihong Meng,1 Xiaopeng Zhang,2 Siyu Wu,1 Mingxia Wu,1 Jing Li,1 Xixin Yan,1 Kamilla Kopec-Harding,3 Jiakai Wu41Respiratory Division, The Second Hospital of Hebei Medical University, 2Department of Thoracic Surgery, Hebei Province General Hospital, Shijiazhuang, Hebei, Peoples’ Republic of China; 3Centre for Musculoskeletal Research, 4Centre for Respiratory and Allergy, Institute of Inflammation and Repair, University of Manchester, Manchester, UKBackground: Systemic inflammation and steroid resistance are the hallmarks of COPD. We examined the impact of p38 inhibitor (SB203580) in in vitro assays of systemic inflammation using pulmonary cells and patients’ sera.Objective and methods: Data from 66 COPD patients and 15 age-/sex-matched healthy controls were compared. Interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and CCL5 were measured in serum samples and culture media from peripheral blood mononuclear cells. The impact of sera on IL-10 and CCL5 expression in alveolar macrophage cell line (MH-S) was examined. The in vitro effects of SB203580 on lipopolysaccharide-induced inflammation were investigated.Results: Peripheral blood mononuclear cells from Global Initiative for Chronic Obstructive Lung Disease (GOLD) D patients produced more CCL5 and TNF-α, and less IL-10 compared to GOLD A–C patients. SB203580 treatment suppressed CCL5 and TNF-α and stimulated IL-10 production; however, the effect of SB203580 on IL-10 was lower in the COPD group. Culture of MH-S cells with COPD serum showed a significant increase in CCL5 and a significant decrease in IL-10 compared to healthy serum. This effect was not suppressed with SB203580 treatment.Conclusion: COPD serum has a potent proinflammatory effect on pulmonary cells. Inhibition of p38 phoshorylation had a limited effect in restoring impaired lymphocyte function and suppressing inflammation induced by COPD serum, implying important p38-independent inflammatory mechanisms in COPD. Keywords: COPD, p38MAPK inhibitor, macrophage, CCL5, TNF-α, IL-10

Fungal endophthalmitis is a serious and vision-threatening infection which requires an immediate and effective treatment approach. Our research aims to elucidate the histological effects of the intravitreal injection of the maximum safe dosage of voriconazole and micafungin on retina. Six albino New Zealand White Rabbits were used. In experimental animals, a solution of voriconazole (Group V) or micafungin (Group M) was intravitreally injected in the right eye, while in control animals, balanced salt solution was intravitreally injected in the left eye (Group C). Euthanasia was performed ten days post injection and the retina was removed and prepared for histological examination with a light and electron microscope. Eosin-hematoxylin staining did not reveal any pathological changes in any of the samples examined. The immunohistochemical staining for Tumor Necrosis Factor alpha (TNF-a) marker was detected as negative in all samples, while Interleukin 6 (IL-6) marker was detected as mild only in the group injected with voriconazole. Electron microscopy revealed several ultrastructural alterations in retinal layers in both groups of experimental animals. Histological retinal lesions, revealed with electron microscopy in the present investigation, raises the question of the safe usage of these antifungal agents in the treatment of fungal intraocular infections in the future.

The increase in the population of older persons needs to be accompanied by increased quality of healthcare in older persons, particularly a decrease in the incidence of infections. Impaired immune responses are common in older adults, and immune senescence likely contributes to the increased incidence of infectious diseases in the older persons. The aging process decreases the immune response and many studies have been conducted to explain the role of supplementation with various micronutrients, such as vitamin C, vitamin E, â-carotene and zinc, on the immune response. The aim of the present study was to assess the influence of 6 months of multi-micronutrient (MMN) supplementation on zinc and tumor necrosis factor (TNF-á) levels in older persons. A randomized controlled trial was conducted on 78 older persons, who were divided into two groups. The treatment group received MMN supplementation containing 40 mg elemental zinc, 120 mg ascorbic acid, 6 mg â-carotene, 15 mg á-tocopherol and 400 ìg folic acid and the control group 400 mg calcium carbonate. The study did not demonstrate that 6 months of MMN supplementation resulted in significant differences between both groups, with respect to total protein, albumin, globulin, and TNF-á levels. In contrast, MMN supplementation significantly decreased the proportion of older persons with zinc deficiency in the treatment group, in comparison with the control group. The present data suggest that in older persons with relatively good immune and protein status, improvement of the immune status by MMN supplementation may be difficult and at best limited.

OBJECTIVE: To evaluate neopterin plasma concentrations in patients with active juvenile idiopathic arthritis (JIA) and correlate them with disease activity.METHODS: Sixty patients diagnosed as active JIA, as well as another 60 apparently healthy age- and gender-matched children as controls, were recruited from the Pediatrics Allergy and Immunology Clinic, Ain Shams University. Disease activity was assessed by the Juvenile Arthritis Disease Activity Score 27 (JADAS-27). Laboratory investigations were performed for all patients, including determination of hemoglobin concentration (Hgb), erythrocyte sedimentation rate (ESR), and C-reactive protein. Serum concentrations of tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and neopterin were measured.RESULTS: Significant differences were found between JIA patients and controls with regard to the mean levels of Hgb, ESR, TNF-a, IL-6, and MCP-1 (p < 0.05). A statistically significant higher mean level serum neopterin concentration (p < 0.05) was found in JIA patients (20.43 ± 8.73 nmol/L) than in controls (6.88 ± 2.87 nmol/L) (p < 0.05). Positive significant correlations were detected between serum neopterin and ESR, TNF-a, IL-6, MCP-1, and JADAS-27 (p < 0.05). No correlation was found between serum neopterin and CRP (p > 0.05). Multiple linear regression analysis showed that JADAS- 27 and ESR were the main variables associated with serum neopterin in JIA patients (p < 0.05).CONCLUSION: The elevation of plasma neopterin concentrations in early JIA patients may indicate stimulation of immune response. Serum neopterin can be used as a sensitive marker for assaying background inflammation and disease activity score in JIA patients.

Metabolic syndrome is a group of several risk factors consist of hypertension, dyslipidemia, glucose intolerance disorder, obesity, and has a relationship with CVD pathomechanism. WHO was report in 2003 more than 300 million adult in the world suffered from obesity. The role of adipose tissue in infectious diseases and adipocyte quality changes after exposure to pathogen has not been revealed. On the other hand, the prevalence of infectious diseases in developing country is still high. Previous studies proved a relationship between infection of Toxoplasma gondii and tissue dysfunction. Profilin is a membrane component of Toxoplasma gondii that able to stimulate expression of proinflammation cytokines through TLR-11 upregulation, and predicted able to trigger the adipocyte dysfunction. The aim of this study are to knows the effect of profilin exposure in vitro on subcutaneous adipocyte to the expression of IL-6 and TNF-α. The measurement of IL-6 and TNF-a levels was done by ELISA technique. The result showed profilin exposure doses 5, 15 and 25 ng / ml increasing IL-6. Profilin exposure cause adipocyte dysfunction through the increasing proinflammatory adipocytokine levels as pathomechanism of metabolic syndrome associated with adipose tissue.

Diabetic retinopathy (DR), a secondary complication of diabetes, is a leading cause of irreversible blindness accounting for 5% of world blindness cases in working age. Oxidative stress and inflammation are considered causes of DR. Curcumin, a product with anti-oxidant and anti-inflammatory properties, is currently proposed as oral supplementation therapy for retinal degenerative diseases, including DR. In this study we predicted the pharmacodynamic profile of curcumin through an in silico approach. Furthermore, we tested the anti-oxidant and anti-inflammatory activity of curcumin on human retinal pigmented epithelial cells exposed to oxidative stress, human retinal endothelial and human retinal pericytes (HRPCs) cultured with high glucose. Because currently marketed curcumin nutraceutical products have not been so far evaluated for their ocular bioavailability; we assessed retinal distribution of curcumin, following oral administration, in rabbit eye. Curcumin (10 μM) decreased significantly (p < 0.01) ROS concentration and TNF-α release in retinal pigmented epithelial cells and retinal endothelial cells, respectively. The same curcumin concentration significantly (p < 0.01) protected retinal pericytes from high glucose damage as assessed by cell viability and LDH release. Among the tested formulations, only that containing a hydrophilic carrier provided therapeutic levels of curcumin in rabbit retina. In conclusion, our data suggest that curcumin, when properly formulated, may be of value in clinical practice to manage retinal diseases. [ABSTRACT FROM AUTHOR]

Background: Many studies have attempted to clarify the association between TNF-a -308G/A polymorphism and pneumoconiosis, but there has been no definite consensus to date. To further assess the effects of TNF-a -308G/A polymorphism on the risk of pneumoconiosis, a meta-analysis was performed in Chinese population. Methods: We searched the related literature in PubMed and Chinese databases through June 2018. The strength of the associations was assessed used pooled odds ratios (ORs) and 95% confidence intervals (CIs). Results: Nine case-control studies including 730 silicosis cases, 457 coal workers pneumoconiosis cases and 2429 controls were identified according to the inclusion criteria. In the total analyses, a significantly elevated risk was found in allelic model (OR = 1.41, 95% CI = 1.16-1.71). In the subgroup analyses by geographic area and type of pneumoconiosis, significant results were found both in North China (A versus G, OR = 1.33, CI = 1.05-1.69) and South China (A versus G, OR = 1.56, CI = 1.14-2.15); significant results were also found in silicosis (A versus G, OR = 1.40, CI = 1.11-1.78) and coal worker pneumoconiosis (A versus G, OR = 1.42, CI = 1.03-1.96). Conclusion: This meta-analysis suggested that TNF-a gene -308 G/A polymorphism is associated with increased silicosis and coal workers pneumoconiosis risk in the Chinese population, and further studies in other ethnic groups are required for definite conclusions. [ABSTRACT FROM AUTHOR]

Heart diseases (HD)in its various form is the leading cause of death worldwide the total number of annual death due to HD is more than 17 million in the world (WHO, 2017). Macrophages display remarkable plasticity, with the ability to undergo dynamic transition between different functional phenotypes. macrophage phenotypes (M1, M2) play important role in heart disease, m1macrophage is pro inflammatory and m2 is anti-inflammatory macrophage. Different cytokines like (interleukins 10,12, and tumor necrosis factor á and interferon gamma) play important role in macrophage polarization (Das et al, 2015). The micro RNAs (miRNA) have been shown to regulate macrophage polarization towered m1 or m2 macrophage and subsequent effects on inflammation in heart diseases ( Liu and Abraham, 2013). The present study was conducted to obtain more clarification of the morphological changes of the macrophage phenotypes in Iraqi patients with heart disease and the factors that predispose them to polarization, such as pro-inflammatory and anti- inflammatory cytokines and role of different factors such as Helicobacter pylori infection and C-reactive protein and the important role of miRNA 146a and miRNA 155 in macrophage polarization. Our study included 80 subjects divided in two groups, the first group was 65 patients with different heart diseases (20 myocardial infraction (MI), 15 heart failer (HF), 10 stable angina (ST angina), and 20 unstable angina (UnST angina)while the second group was 15 healthy volunteers, serum was collected from thesegroups. for quantification of serum IL10, IL12, TNF- á and IFN-ã level by ELISA technique, furthermore detection the Helicobacter pylori antibody by using rapid test and agglutination test to estamination of C- reactive protein (CRP)in serum, in addition miRNA was extracted from serum samples and qRT-PCR was carried out to detect the expression level of miRNA 155 and miRNA 146 in patient and control. The ELISA results show highly significance(PÂ0.01) increment of interleukin IL-10 and significantly increased of tumor necrosis factor alpha (TNF-á) (PÂ0.01), and also showed significantly decreased level of interleukin 12(IL-12), and interferon gamma (IFN-ã). By using qRT-PCR the result show highly significance expression of miRNA 146a and miRNA 155 in serum of study groups. The highly increased of anti-inflammatory (IL10) and TNF-á and low level of some proinflammatory is associated with highly expression of miRNA146a and low increased of miRNA 155 in all study groups compared with miRNA 146a expression, reflect the important role of miRNA in macrophage polarization. [ABSTRACT FROM AUTHOR]

Aim. To study the clinical and predictive importance of polymorphism of rs1800629 (G-308A) of TNF gene in patients with STEMI.Material and methods. Research included patients (171 persons with STEMI), hospitalized to the Kemerovo cardiological center and 188 individuals without the diagnosed cardiovascular diseases. In all patients the genotype had the polymorphism of rs1800629 of TNF gene. Investigation was carried out with help the original DNA microarray.Results. Associations of the rs1800629 (G-308A) polymorphic variant in the TNF gene with the concentration of the tumor necrosis factor alpha (TNFa) in the blood serum and cardiovascular complications in patients with myocardial infarction with the elevated ST segment (MIST) have been studied. Allele A rs1800629 frequency in patients with MIST (n=171) was 11,7% which did not differ from the frequency in healthy controls (n=188) – 12,2%. Allele A careerstatus was associated with the higher levels of the TNFa concentration in the blood serum measured at the day 10th-14th after MI: 11,02 pg/ml compared to 9,49 in G homozygotes (p=0,045). While analyzing the clinical status of MIpatients after one year follow up, it was revealed that A allele has the frequency 19% in patients with progressive angina pectoris (AP) compared to 10% in patients without progressive AP, and 16% in patients with cardiovascula rcomplications (CVC) such as repeated MI, stroke, instable AP or death from cardiovascular reasons compared to 9% frequency in patients without CVC, which was not statistically significant. We had shown in earlier s tudy that TNFa high level in patients with MI is related to the risk of CVC. Although, in current study we did not detect an association of the rs1800629 with progression of the AP, chronic heart failure decompensation, CVC or death from cardiovascularreasons in one year after IM. Thus, rs1800629 allele A does influence TNFa concentrations, but there is no data supporting the fact that this variant is an independent risk factor for IM and its complications.Conclusion. The results indicate possible predictive value of rs1800629 polymorphism of TNF gene to predict the cardiovascular events in patients with STEMI during 12 months of follow up.

Objective. To investigate the correlation among pro- or anti-inflammatory cytokines and the two main gut microbiota phyla in obese children. Materials and methods. Anthropometric data were obtained from 890 children under 14 years old to determine the degree of obesity. Serum cytokine concentration was measured by ELISA. Relative abundance of gut microbiota in feces was evaluated by quantitative Real-Time PCR assays. Results. Anthropometric and biochemical parameters were statistically higher in overweight/obese children than in lean ones. Increased TNF-a levels were found in obese children that also have a high relative abundance of Firmicutes. Conclusions. Obese children have a high relative abundance of Firmicutes that correlates with increased levels of TNF-a. This is the first study that shows a relation between Firmicute abundance and TNF-a serum concentration in obese children. [ABSTRACT FROM AUTHOR]

Background: Macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine with chemokine-like functions, has been shown to play a central role in several acute and chronic inflammatory diseases. However, limited information is available regarding the use of MIF as an inflammatory pathway marker in patients with tuberculosis. This study aimed to investigate the association of MIF with IFN-γ and TNF-α in active pulmonary tuberculosis (APTB) following anti-tuberculosis treatment. Methods: The MIF, TNF-α, and IFN-γ serum levels were determined in 47 patients with APTB by cytokine-specific ELISA at four phases: prior to anti-tuberculosis drug treatment (baseline), and following 2, 4, and 6 months of treatment. In addition, we measured the MIF, TNF-α, and IFN-γ serum levels in 50 health controls. Results: MIF serum levels were significantly elevated (P <0.05) in patients with APTB prior to treatment compared with that in control subjects, and TNF-α ≥449.7 pg/mL was associated with high MIF levels (≥13.1 ng/mL). MIF levels were significantly reduced (P <0.01) following 2, 4, and 6 months of treatment, with variations in TNF-α and IFN-γ serum levels. MIF levels were positively correlated with the paired TNF-α level at baseline (r=0.1103, P =0.0316) and following 6 months of treatment (r=0.09569, P =0.0364). Conclusions: A reduction in the MIF serum levels in patients with APTB following anti-tuberculosis treatment may positively affect host immune protection against Mycobacterium tuberculosis infection. Thus, serum MIF levels may constitute a useful marker for assessing therapy effectiveness in patients with APTB. [ABSTRACT FROM AUTHOR]

Background: Pigment-grade titanium dioxide (TiO2) particles are an additive to some foods (E171 on ingredients lists), toothpastes, and pharma-/nutraceuticals and are absorbed, to some extent, in the human intestinal tract. TiO2 can act as a modest adjuvant in the secretion of the pro-inflammatory cytokine interleukin 1β (IL-1β) when triggered by common intestinal bacterial fragments, such as lipopolysaccharide (LPS) and/or peptidoglycan. Given the variance in human genotypes, which includes variance in genes related to IL-1β secretion, we investigated whether TiO2 particles might, in fact, be more potent pro-inflammatory adjuvants in cells that are genetically susceptible to IL-1β-related inflammation. Methods: We studied bone marrow-derived macrophages from mice with a mutation in the nucleotide-binding oligomerisation domain-containing 2 gene (Nod2m/m), which exhibit heightened secretion of IL-1β in response to the peptidoglycan fragment muramyl dipeptide (MDP). To ensure relevance to human exposure, TiO2 was food-grade anatase (119 ± 45 nm mean diameter ± standard deviation). We used a short 'pulse and chase' format: pulsing with LPS and chasing with TiO2 +/- MDP or peptidoglycan. Results: IL-1β secretion was not stimulated in LPS-pulsed bone marrow-derived macrophages, or by chasing with MDP, and only very modestly so by chasing with peptidoglycan. In all cases, however, IL-1β secretion was augmented by chasing with TiO2 in a dose-dependent fashion (5-100 µg/mL). When co-administered with MDP or peptidoglycan, IL-1β secretion was further enhanced for the Nod2m/m genotype. Tumour necrosis factor a was triggered by LPS priming, and more so for the Nod2m/m genotype. This was enhanced by chasing with TiO2, MDP, or peptidoglycan, but there was no additive effect between the bacterial fragments and TiO2. Conclusion: Here, the doses of TiO2 that augmented bacterial fragment-induced IL-1β secretion were relatively high. In vivo, however, selected intestinal cells appear to be loaded with TiO2, so such high concentrations may be 'exposure-relevant' for localised regions of the intestine where both TiO2 and bacterial fragment uptake occurs. Moreover, this effect is enhanced in cells from Nod2m/m mice indicating that genotype can dictate inflammatory signalling in response to (nano)particle exposure. In vivo studies are now merited. [ABSTRACT FROM AUTHOR]

Background: Mesenchymal stromal cells (MSCs) can be used intra-articularly to quell inflammation and promote cartilage healing; however, mechanisms by which MSCs mitigate joint disease remain poorly understood. Galectins, a family of ß-galactoside binding proteins, regulate inflammation, adhesion and cell migration in diverse cell types. Galectin-1 and galectin-3 are proposed to be important intra-articular modulators of inflammation in both osteoarthritis and rheumatoid arthritis. Here, we asked whether equine bone marrow-derived MSCs (BMSCs) express higher levels of galectin-1 and -3 relative to synovial fibroblasts and chondrocytes and if an inflammatory environment affects BMSC galectin expression and motility. Methods: Equine galectin-1 and -3 gene expression was quantified using qRT-PCR in cultured BMSCs, synoviocytes and articular chondrocytes, in addition to synovial membrane and articular cartilage tissues. Galectin gene expression, protein expression, and protein secretion were measured in equine BMSCs following exposure to inflammatory cytokines (IL-1ß 5 and 10 ng/mL, TNF-a 25 and 50 ng/mL, or LPS 0.1, 1, 10 and 50 µg/mL). BMSC focal adhesion formation was assessed using confocal microscopy, and BMSC motility was quantified in the presence of inflammatory cytokines (IL-1ß or TNF-a) and the pan-galectin inhibitor ß-lactose (100 and 200 mM). Results: Equine BMSCs expressed 3-fold higher galectin-1 mRNA levels as compared to cultured synovial fibroblasts (p = 0.0005) and 30-fold higher galectin-1 (p < 0.0001) relative to cultured chondrocytes. BMSC galectin-1 mRNA expression was significantly increased as compared to carpal synovial membrane and articular cartilage tissues (p < 0.0001). IL-1ß and TNF-a treatments decreased BMSC galectin gene expression and impaired BMSC motility in dose-dependent fashion but did not alter galectin protein expression. ß-lactose abrogated BMSC focal adhesion formation and inhibited BMSC motility. Conclusions: Equine BMSCs constitutively express high levels of galectin-1 mRNA relative to other articular cell types, suggesting a possible mechanism for their intra-articular immunomodulatory properties. BMSC galectin expression and motility are impaired in an inflammatory environment, which may limit tissue repair properties following intra-articular administration. ß-lactose-mediated galectin inhibition also impaired BMSC adhesion and motility. Further investigation into the effects of joint inflammation on BMSC function and the potential therapeutic effects of BMSC galectin expression in OA is warranted. [ABSTRACT FROM AUTHOR]

Background: rheumatoid arthritis (RA) is a chronic inflammatory arthropathic with multiorgan involvement. Increased prevalence of insulin resistance (IR) has been observed in patients with RA. Highgrade systemic inflammation is implicated in the development of IR in these patients. Tumor necrosis factoralpha (TNF-α) is a potent proinflammatory cytokine that plays a role in initiation and progression of inflammation and the mechanisms associated with accelerated atherosclerosis in RA. Aim of the work: this study aimed to investigate the relation between TNF-α and IR in RA patients and its relation to disease activity. Patients and methods: 40 RA patients were included as the patient group and 40 healthy subjects as the control group. Both groups were subjected to full history, clinical examination including body mass index (BMI) and lab investigation, fasting blood glucose, fasting insulin and TNF-α. Results: the sex distribution was the same in patients and the control groups, 82.5% females and 17.5% males. The disease activity (DAS score) was 4.57 ± 1.35. TNF-α median was 240 with IQR 190-510. RA patients had significantly higher serum TNF-α than controls (p value = 0.001). BMI and Waist Circumference among RA patients and controls showed no significant difference. TNF-α has significantly positive correlations with fasting serum insulin, HOMA-IR and disease activity in RA patient group (p value < 0.001). Conclusion: serum TNF-α level was significantly higher in RA patients than the control groups with positive correlation in fasting serum insulin, HOMA score and disease activity. [ABSTRACT FROM AUTHOR]

The aim of the work is determination of intercommunication of cytokines IL-10, 1L-6 levels, TNF-a with subjective estimation of pain, processes of the nervous system desadaptation in patients with genital endometriosis in combination with benign hormonal pathology of the genitalia followed by chronic pelvic pain (CPP). There were 120 women in research divided into several groups, depending on visual analogue scale (VAS) and durations o f disease: 1st group (n=44), VAS was 7-10 points; 2-d group (n=41) VAS - 4-6 points; 3-d group (n=35) VAS - 0-3 points. Along with progress o f CPP there was marked decline of cytokines IL-10, and increase of IL-6, TNF -a comparatively with 3-d group (p<0,05); this correlated with the higher points of intensity of pain syndrome in the 1st group, with pain anamnesis duration and increased level of anxiety and depression. Imbalance of cytokines towards the proinflammatory link in definite clinical provoking factors of pain can be considered as a predictor of CPP. [ABSTRACT FROM AUTHOR]

Background: Many factors contribute for viral clearance and response to antiviral therapy. Genetic polymorphisms of cytokines, chemokines, and their receptors can alter the immune response against Hepatitis C virus (HCV). Aim of the study: The aim of the current study is to assess single nucleotide polymorphism (SNP) in the promoter region of IL-10, TNF-α, IFN-ώ and TGF-β as predictors of response to combined Pegylated interferon a/ribavirin (PEG-IFN/RBV) therapy in chronic HCV infected Egyptian patients. Patients and methods: The study was conducted on 150 HCV infected patients and 100 apparently healthy control subjects. All patients were treated with PEG-IFN/RBV. They were classified according to their response to treatment. Genotyping of IL-10, TNF-α, IFN-ώ and TGF-β were performed on peripheral blood DNA using polymerase chain reaction-restriction fragment-length polymorphism (PCR-RFLP) and primer specific assays. Results: Overall, 83/150 (55.3%) patients achieved sustained virological response (SVR), whereas 67 (44.7%) did not. Age and BMI were significantly lower in patients who achieved SVR (P<0.05). IL-10 at site (±1082) GG genotype was associated with SVR where odds ratio was 1.98 with 95% confidence interval (1.34-3.65). None of the other genes showed a significant association with SVR. Conclusion: Analysis of IL-10 SNP at promoter site (±1082) could be used as a pretreatment predictor of response to combined PEG-IFN/RBV treatment. [ABSTRACT FROM AUTHOR]

Objective:The purpose of this study was to evaluate levels of interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in gingival crevicular fluid (GCF) with hybrid and PG retractors, which have differences in constancy of force.Materials and Method:Forty canine teeth of 10 orthodontic patients were distalized with hybrid or PG retractors. The GCF was sampled from the distal sides of the canines at baseline, hour 1, day 1, month 1, and month 2. In the PG group, samples were re-collected 1 hour and 1 day after reactivation at month 1. Two-way ANOVA, paired t test, and Friedman and Wilcoxon tests were used for statistical analysis.Results:The IL-1β level increased at hour 1 and month 2 in the upper and lower hybrid groups, whereas upper PG group increased at hour 1, month 1 + 1 hour, and month 2. The TNF-α level increased at hour 1 and declined afterward in the upper hybrid group. The only difference between the 2 retractors was found in TNF-α levels, which were higher at day 1 and month 2 in the upper PG group.Conclusion:Continuous but diminishing forces produced by PG mechanics enhanced levels of TNF-α significantly at day 1 and month 2 compared with the constant and continuous forces applied by the hybrid retractor in the upper arch. Despite this difference, both retractors induced similar effects in IL-1β and TNF-α production and in the amount of tooth movement.

Inflammation contributes to cognitive impairment in patients with hepatic encephalopathy (HE). However, the process by which peripheral inflammation results in cognitive impairment remains unclear. In animal models, neuroinflammation and altered neurotransmission mediate cognitive impairment. Taking into account these data, we hypothesized that in rats with HE: 1) peripheral inflammation is a main contributor to neuroinflammation; 2) neuroinflammation in hippocampus impairs spatial learning by altering AMPA and/or NMDA receptors membrane expression; 3) reducing peripheral inflammation with infliximab (anti-TNF-a) would improve spatial learning; 4) this would be associated with reduced neuroinflammation and normalization of the membrane expression of glutamate receptors. The aims of this work were to assess these hypotheses. We analyzed in rats with portacaval shunt (PCS) and control rats, treated or not with infliximab: a) peripheral inflammation by measuring prostaglandin E2, IL10, IL-17 and IL-6;b) neuroinflammation in hippocampus by analyzing microglial activation and the content of TNF-a and IL-1b, IL-1b), c) AMPA and NMDA receptors membrane expression in hippocampus and d) spatial learning in the Radial and Morris water mazes. We assessed the effects of treatment with infliximab on peripheral inflammation, on neuroinflammation and AMPA and NMDA receptors membrane expression in hippocampus and on spatial learning and memory.PCS rats show increased serum prostaglandin E2, IL-17 and IL-6 and reduced IL-10 levels, indicating increased peripheral inflammation. PCS rats also show microglial activation and increased nuclear NF-kB and expression of TNF-a and IL-1b in hippocampus. This was associated with altered AMPA and NMDA receptors membrane expression in hippocampus and impaired spatial learning and memory in the radial and Morris water maze.Treatment with infliximab reduces peripheral inflammation in PCS rats, normalizing prostaglandin E2, IL-17, IL-6 and IL-10 levels in serum. Infliximab also prevents neuroinflammation, reduces microglial activation, translocates NF-kB into nucleoli and normalizes TNF-a and IL-1b content in hippocampus. This was associated with normalization of AMPA receptors membrane expression in hippocampus and of spatial learning and memory. The results suggest that peripheral inflammation contributes toispatial learning impairment in PCS rats. Treatment with anti-TNF-a could be a new therapeutic approach to improve cognitive function in patients with HE.

Inflammatory responses and innate immunologic reactions play an important role in the respiratory system. Ex vivo lung perfusion (EVLP) is considered a novel method in the evaluation and reconditioning of donor lungs prior to transplantation. However, EVLP’s effect on inflammatory and metabolic markers of human lung tissue is unknown. This study investigated how the performance of EVLP on brain-dead (BD) donor lungs affects the production and release of inflammatory cytokines (IL-6, IL-8, and TNF-a), inflammatory cells and toll-like receptors (TLR) -2, 4. This study was conducted with an animal subject for qualification of EVLP team and then EVLP was performed on 4 human cases referred to Masih Daneshvari Hospital (Tehran,Iran), from May 2013 to July 2015. Two of these cases, who had acceptable lung function parameters, were enrolled in this study for immunologic investigations. Bronchoalveolar lavages (BAL) were taken before and after EVLP. Cytokines were quantitatively measured before lung retrieval, at the end of the lung removal, at the start of EVLP, and at the end of the each hour of EVLP. TLR expression was measured on the cells obtained by flow cytometry. TNF-a, IL-6 and IL-8 decreased in each stage of washing perfusate in both cases, and the level of cytokines in serum was in the normal range. Flow cytometry analysis revealed a decreasing expression of CD3, CD4/8, CD19, and CD16+56, as well as TLR-2 and TLR-4 in both cases. Intra-capillary pools of pro-inflammatory cytokines (IL-6, IL-8, and TNF-a) were determined to contribute to the lung injury during prolonged lung perfusion. This raises the possibility that EVLP donor lungs could be less immunogenic than standard lungs. However, to assess EVLP’s effects on lung grafts and optimize recipient outcomes, further studies with a sufficient number of lungs are required.

En la actualidad se ha mostrado interés en el empleo de la saliva para ser utilizada como una alternativa de diagnóstico, predicción y progresión de diversas enfermedades con relación a otros fluidos corporales. Los objetivos trazados para la realización de este trabajo fueron: correlacionar las concentraciones en saliva y sangre de IL-1, IL-6, TNF-a, sustancias reactivas al ácido tiobarbitúrico y O2- de niños y adolescentes sistémicamente sanos. Se realizó un estudio de corte transversal en 23 niños y adolescentes sanos, entre 4 y 17 años de edad. Se les realizaron evaluaciones clínicas para determinar las condiciones bucales y estudios inmunológicos con el propósito de identificar los niveles de citosinas, a través del ensayo inmunoenzimático indirecto, el O2- por método citoquímico y las sustancias reactivas al ácido tiobarbitúrico, a través del ensayo colorimétrico. Hubo diferencia significativa entre las muestras de saliva y las de sangre periférica respecto a las citosinas y sustancias reactivas al ácido tiobarbitúrico estudiadas. Los resultados fueron: IL-1 en sangre= 1,646 ± 0,13 pg/mL y de IL-1 en saliva= 552,36 ± 75,7 pg/mL; IL-6 en sangre= 3,506 ± 1,85 pg/mL, e IL-6 en saliva= 26,89 ± 9,97 pg/mL. Al analizar el TNF-a en sangre fue de 12,91 ± 3,05 pg/mL y en saliva= 43,56 ± 6,44 pg/mL, las sustancias reactivas al ácido tiobarbitúrico en sangre= 9,46 ± 3,26 nmol/mL y en saliva= 1,26 ± 0,03 nmol/mL. No se observó correlación estadísticamente significativa entre las muestras de sangre y saliva para los valores de IL-1, IL-6 y sustancias reactivas al ácido tiobarbitúrico. En cuanto al TNF-a se evidenció una correlación significativa, r s= 0,78. No se evidenciaron células positivas para el O2- en las muestras estudiadas. Los resultados del análisis de correlación obtenido entre las muestras salivales y séricas, no aportaron evidencias suficientes para sugerir que la saliva pueda ser utilizada como fluido corporal que permita sustituir la determinación sérica de IL-1, IL-6 y sustancias reactivas al ácido tiobarbitúrico. En cuanto al TNF-a se evidenció una correlación significativa, lo cual podría plantear la posible sustitución de muestras séricas por salivales.At present times, there is interest in the use of saliva as a diagnosis, prediction and progression alternative of different pathologies in relation to the body fluids. To correlate the concentrations of IL-1, IL-6, TNF-a, substances reactive to thiobarbituric acid (RSTBA) and O2- in the saliva and blood of systematically healthy children and adolescents. A cross-sectional study was performed in 23 healthy children and adolescents aged from 4 to 17 underwent to clinical tests to demonstrate the oral conditions and immunological to identify the cytokine levels and the RSTBAs by colorimetry trial. There was a significant difference in saliva samples compared to that of peripheral blood in study cytokines and RSTBAs: IL-1 (blood: 1.646 ± 0.13 pg/mL, saliva: 552.36 ± 75.7 pg/mL; IL-6 (blood: 3.506 ± 1.85 pg/mL, saliva: 26.89 ± 9.97 pg/mL: TNF-a (blood: 12.91 ± 3.05 pg/mL, saliva: 43.56 ± 6.44 pg/mL), RSTBA (blood: 9.46 ± 3.26 nmol/mL, saliva: 1.26 ± 0.03 nmol/mL). There was not a statistically significant difference among blood and saliva samples for IL-1, IL-6 and RSTBA values. As regards TNF-a it was demonstrated a significant correlation, r s= 0.78. There was not evidence of cells positive to O2 in study samples. Results of correlation analysis obtained among the saliva and serum samples not offer evidences that saliva may be used as body fluid allows substituting the serum determination of IL-1, IL-6 and RSTBA. In the case of the TNF-a, there was a significant correlation, which could to propose the possible substitution of serum samples for the salivary ones.

The increase in the population of older persons needs to be accompanied by increased quality of healthcare in older persons, particularly a decrease in the incidence of infections. Impaired immune responses are common in older adults, and immune senescence likely contributes to the increased incidence of infectious diseases in the older persons. The aging process decreases the immune response and many studies have been conducted to explain the role of supplementation with various micronutrients, such as vitamin C, vitamin E, â-carotene and zinc, on the immune response. The aim of the present study was to assess the influence of 6 months of multi-micronutrient (MMN) supplementation on zinc and tumor necrosis factor (TNF-á) levels in older persons. A randomized controlled trial was conducted on 78 older persons, who were divided into two groups. The treatment group received MMN supplementation containing 40 mg elemental zinc, 120 mg ascorbic acid, 6 mg â-carotene, 15 mg á-tocopherol and 400 ìg folic acid and the control group 400 mg calcium carbonate. The study did not demonstrate that 6 months of MMN supplementation resulted in significant differences between both groups, with respect to total protein, albumin, globulin, and TNF-á levels. In contrast, MMN supplementation significantly decreased the proportion of older persons with zinc deficiency in the treatment group, in comparison with the control group. The present data suggest that in older persons with relatively good immune and protein status, improvement of the immune status by MMN supplementation may be difficult and at best limited.

The aim of this research in to investigate the anticytokine activities of the 2-[(2-nitro-l-phenylpropyl)thio]benzoic acid (1), 2-[(2-nitro-l-phenylethyl)thiomethyl]benzimidazole (2) and 2-[(2-nitro-l-phenylpropyl)thiomethyl]benzimidazole (3) derivatives in human primary cells and cell lines. Cytokines are messengers for the regulation of the inflammatory cascades with Tumor Necrosis Factor-a (TNF-a), Interleukin (IL-lβ, IL-2, IL-4 andIL-8), Gamma Interferon (IFN-y) working synergistically. In this study which is performed in cell assay, inhibition capacity of compound 1, 2 and 3 derivatives againts TNF-a, IL-Iβ, IL-8, IL-2, IL-4 and IFN-y production by human whole blood have been measured. The test results were shown that 1, 2 and 3 derivatives have dose-dependent inhibitions on the release of IL-1β, IL-8 and TNF-a in lipopolysaccharide (LPS) stimulated human whole blood and IL-2, IL-4 and IFN-yin phorbolacetate (PHA) stimulated in human whole blood

Immunomodulatory treatment of chronic rhinosinusitis with nasal polyposis (CRSwNP) by macrolide antibiotics represents a challenging alternative to conventional therapy and surgery, still being at the very beginning. Immune and inflammatory processes in nasal and paranasal sinus mucosa, crucial in the etiopathogenesis of nasal polyps (NPs) are reflected in levels of various local mediators, found both in mucosa and nasal fluid. In this prospective study, we assessed the immunomodulatory and clinical effects of longterm low-dose oral macrolide treatment in the management of CRSwNP. Twenty-two (n = 22) nonasthmatic, nonallergic patients with CRSwNP were administered clarithromycin (CAM) 500 mg/day single oral dose for eight weeks. We measured the levels of proinflammatory cytokines TNF-a, TNF-b, and IL-1b, Th1 cytokines IL-2, IL-12, and IFN-g, Th2 cytokines IL-4, IL-5, IL-6, and IL-10, and chemokine IL-8 in the nasal fluid samples, before and after treatment, using a flow cytometric method. We also scored each of the 22 patients before and after therapy according to Tsicopoulos' global nasal symptom score and Malm's endoscopic score. Following treatment, we found significantly reduced levels of IL-8 (p