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OBJECTIVE: To explore the impact of vitamin D deficiency (VD-) in the pathogenesis of metabolic syndrome (MetS). MATERIALS AND METHODS: Models of (VD-) and (MetS) were induced in male Wister rats by dividing into four groups, group-I for the development of (VD-) by intraperitoneal injection of paricalcitol for 3 weeks, group II for (MetS) model by adding 10% fructose to their drinking water for 8 weeks, the group III for induction of combined (VD- + MetS) and group-IV as a control. Ultimately, the parameters of (VD-) and (MetS) were assessed at zero time and after 8 weeks. RESULTS: Both (VD-) and (MetS) groups alone displayed a remarkable enhancement of blood pressure, glucose and insulin levels, triglycerides, cholesterol, and low-density lipoproteins with a reduction of high-density lipoproteins. Additionally, all distinguishing features of obesity were substantially increased. Nevertheless, the combined group (VD-+MetS) demonstrated an expeditious and substantial increase in all the aforesaid parameters compared to the (VD-) and (MetS) groups alone. CONCLUSIONS: The hallmark of this study, reinforces a new frontier of awareness of the deleterious effect of (VD-) on each component of (MetS). Eventually, supplementation of vitamin D can circumvent the elements of (MetS) and needs further validation by determination of (VD-) molecular pathway on the parameters of (MetS). [ABSTRACT FROM AUTHOR]

On one side, decompression sickness (DCS) with neurological disorders lead to a reshuffle of the cecal metabolome of rats. On the other side, there is also a specific and different metabolomic signature in the cecum of a strain of DCS-resistant rats, that are not exposed to hyperbaric protocol. We decide to study a conventional strain of rats that resist to an accident-provoking hyperbaric exposure, and we hypothesize that the metabolomic signature put forward may correspond to a physiological response adapted to the stress induced by diving. The aim is to verify and characterize whether the cecal compounds of rats resistant to the provocative dive have a cecal metabolomic signature different from those who do not dive. 35 asymptomatic diver rats are selected to be compared to 21 rats non-exposed to the hyperbaric protocol. Because our aim is essentially to study the differences in the cecal metabolome associated with the hyperbaric exposure, about half of the rats are fed soy and the other half of maize in order to better rule out the effect of the diet itself. Lower levels of IL-1β and glutathione peroxidase (GPX) activity are registered in blood of diving rats. No blood cell mobilization is noted. Conventional and ChemRICH approaches help the metabolomic interpretation of the 185 chemical compounds analyzed in the cecal content. Statistical analysis show a panel of 102 compounds diet related. 19 are in common with the hyperbaric protocol effect. Expression of 25 compounds has changed in the cecal metabolome of rats resistant to the provocative dive suggesting an alteration of biliary acids metabolism, most likely through actions on gut microbiota. There seem to be also weak changes in allocations dedicated to various energy pathways, including hormonal reshuffle. Some of the metabolites may also have a role in regulating inflammation, while some may be consumed for the benefit of oxidative stress management. [ABSTRACT FROM AUTHOR]

On one side, decompression sickness (DCS) with neurological disorders lead to a reshuffle of the cecal metabolome of rats. On the other side, there is also a specific and different metabolomic signature in the cecum of a strain of DCS-resistant rats, that are not exposed to hyperbaric protocol. We decide to study a conventional strain of rats that resist to an accident-provoking hyperbaric exposure, and we hypothesize that the metabolomic signature put forward may correspond to a physiological response adapted to the stress induced by diving. The aim is to verify and characterize whether the cecal compounds of rats resistant to the provocative dive have a cecal metabolomic signature different from those who do not dive. 35 asymptomatic diver rats are selected to be compared to 21 rats non-exposed to the hyperbaric protocol. Because our aim is essentially to study the differences in the cecal metabolome associated with the hyperbaric exposure, about half of the rats are fed soy and the other half of maize in order to better rule out the effect of the diet itself. Lower levels of IL-1β and glutathione peroxidase (GPX) activity are registered in blood of diving rats. No blood cell mobilization is noted. Conventional and ChemRICH approaches help the metabolomic interpretation of the 185 chemical compounds analyzed in the cecal content. Statistical analysis show a panel of 102 compounds diet related. 19 are in common with the hyperbaric protocol effect. Expression of 25 compounds has changed in the cecal metabolome of rats resistant to the provocative dive suggesting an alteration of biliary acids metabolism, most likely through actions on gut microbiota. There seem to be also weak changes in allocations dedicated to various energy pathways, including hormonal reshuffle. Some of the metabolites may also have a role in regulating inflammation, while some may be consumed for the benefit of oxidative stress management.

Sepsis is considered the leading cause of death in emergency units. It is known that there are already serum immune parameters/biomarkers useful in predicting the progression from peritonitis to sepsis, respectively septic shock. In the present study, we aimed to measure the serum concentrations of CASP1, CRP and cytokines (IL-23, IL-1β, IL-18); to compare immune-inflammatory cell ratios at the onset of peritonitis, before and after sepsis; to identify correlations between the concentration of the CASP1, IL-23, IL-1β, IL-18, CRP, ESR and the indices that assess the prognosis of patients with peritonitis (MPI) and the severity of sepsis (SOFA, APACHE II) and with different ratios of immunocytes (NLR, MLR, PltLR) and to investigate the usefulness of these immune parameters in predicting the progression from peritonitis to sepsis using the area under the ROC curve. Serum samples were collected from 20 peritonitis patients diagnosed and 14 patients who developed secondary sepsis to peritonitis. For the evaluation of serum concentrations of studied mediators, we used immunoenzymatic technique. In our study, we obtained significantly increased values in the serum of patients who developed sepsis vs the group with peritonitis, for CASP1, CRP and cytokines (IL-23, IL-1β, IL-18). Serum levels of CASP1 correlated much better with the evaluated indices, statistically significant correlations. Two markers investigated, CASP1 and IL-23, had a diagnostic accuracy (71.10% and 70.90%, respectively) almost similar to the performance of IL-1β (accuracy of 71.40%), in the diagnosis of peritonitis. In conclusion, the investigated serological markers (CASP1, IL-23, IL-1β, IL-18) can be used as an independent prognostic markers for differentiation of patients with peritonitis from those with sepsis, in combination with CRP, ESR, NLR and the indices (MPI, SOFA, APACHE II). [ABSTRACT FROM AUTHOR]

Die Zeiten, in denen nur Laktat und Kreatinkinase als blutbasierte Biomarker für die Belastungssteuerung zur Verfügung standen, sind lange vorbei. Heutzutage steht eine große Anzahl von Biomarkern aus Blut, Urin und Spei)chel zur Verfügung. Ob deren Einsatz zusätzlich zu Trackingsystemen und Fragebögen sinnvoll ist, sollte sorgfältig geprüft werden. Sowohl die Probenentnahme und die Analyse als auch die Interpretation der generierten Daten erfordern Expertise. [ABSTRACT FROM AUTHOR]

Introduction: Cytokines are responsible for regulating tissue reactions in periodontal disease. An imbalance between pro- and anti-inflammatory cytokines can cause favorable conditions for onset and progression of chronic periodontitis. The aim of the study was to evaluate associations between IL4, IL6 and TNF-α and assess plasmatic variations of these cytokines in patients with different stages of chronic periodontitis. Material and method: The study included 77 subjects, 31 males and 46 females with different stages of chronic periodontitis which were divided into 4 groups: healthy group (HG), early generalized chronic periodontitis (EGP), moderate generalized chronic periodontitis (MGP) and advanced generalized chronic periodontitis (AGP). Evaluation of plasmatic levels of IL4, IL6 and TNF-α was performed using enzyme-linked immunosorbent assay (ELISA) test. Results: Plasmatic levels of IL6 and TNF-α were elevated in the MGP and AGP groups compared to the healthy and EGP group and IL4 levels were higher in healthy subjects than in chronic periodontitis subjects. Significant positive correlations were found between IL6 and TNF-α in advanced stages of chronic periodontitis and negative correlations were found between IL4 and TNF-α during chronic periodontitis progression. Conclusions: Increased plasmatic concentrations of IL6 and TNF-α proinflammatory cytokines along with progression of chronic periodontitis may be relevant for a systemic proinflammatory status. The direct proportional relationship between IL6 and TNF-α proinflammatory cytokines and inversed ratio to IL4 anti-inflammatory interleukin in chronic periodontitis highlights a strong influence of the immune system on the progression of this disease. [ABSTRACT FROM AUTHOR]

Copyright of Der Hautarzt is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Single Nucleotide Polymorphisms (SNPs) of IL 28 B and IL 10 were associated with sustained virological response (SVR) and liver fibrosis in chronic hepatitis C patients treated with peg-interferon (Peg IFN) and Ribavirin (RBV). Methods: We studied 188 patients with chronic hepatitis C who received antiviral therapy. RNA HCV was determined by RT-PCR and liver fibrosis was evaluated by transient elastography (Fibroscan) and serological tests (APRI score). The IL 28 B rs12979860 and IL 10 R -1087 (rs1800896) SNPs were genotyped using Custom Taqman SNP Genotyping Assays. Results: From 176 patients, 98 (55.68%) had SVR, 59 (33.52%) were nonresponders and 19 (10.80%) were relapsers. SVR was strongly associated with IL 28 B SNP genotypes (p<0.0005). Advanced/severe fibrosis was observed in 109 cases (57.97%). Fibrosis was not associated with IL 28 B SNP. IL 10 R SNP was a predictor for liver fibrosis: severe fibrosis was present in 66.67% of patients with GG genotype, 26.98% with GA and 51.02% with AA genotypes. The G allele of IL-10 SNP was associated with advanced fibrosis (OR: 2.40, p = 0.018). Conclusions: The determination of the interleukins polymorphisms is important in predicting the viral response to interferon therapy and evolution of liver fibrosis. [ABSTRACT FROM AUTHOR]

Introducere: Sepsisul este o boala caracterizată printr-un răspuns sistemic inflamator cauzat o infecție care poate evolua către sepsis sever și șoc septic. Această patologie ridică mari probleme la nivel global din cauza mortalității ridicate (care în anumite situații atinge 30%) precum și din cauza încarcăturii financiare mari. Sepsisul se caracterizează prin declasnșarea unor căi imune pro-inflamatorii cu rol de apărare a organismului dar care ulterior se dovedesc a fi extrem de dezajantajoase. Deși antibioterapia, resuscitarea volemică, terapia vasopresoare și controlul sursei de infecție rămân strategiile recomandate în tratamentul sepsisului, date publicate recent propun statinele ca o noua linie de tratament. Aceste medicamente au fost introduse în practica clinică datorită efectului hipocolesterolemiant însă inhibarea reductazei HMG-CoA și a biosintezei colesterolului induce o serie de efecte mai puțin studiate denumite generic pleiotrope: anti-inflamatoare, antitrombotice, imunomodulatoare și antioxidante. Obiective: În cadrul acestui experiment ne-am propus să evaluăm și să comparăm efectul antiinflamator al Simvastatinei și Rosuvastatinei măsurând nevelele serice ale IL-1β, IL-6 și TNF-α folosind un model consacrat de sepsis la șobolan. Metode: Am alcătuit patru grupuri (C, n=7; SEP, SV, RV, n=8). Statinele au fost administrate în două doze cu 18 și 3 ore înaintea intervenției chirurgicale. Sepsisul a fost obținut prin tehnica ligaturării și puncției cecale. De la fiecare subiect au fost recoltate eșantioane de sânge prin puncție venoasă în zilele 1, 4, 7 și 14 (ultimele eșantioane au fost obținute prin puncție cardiacă). Au fost analizați următorii parametrii: hemoleucograma, Procalcitonina, IL-1β, IL-6 și TNF-α. Rezultate: Numărul total al leucocitelor a fost mai mare pentru grupul septic dar netratat. Procalcitonina a fost reacționată în toate grupurile septice însă valori mai mici au fost observate în grupurile tratate cu Simvastatină și Rosuvastatină în comparație cu grupul netratat. Nivelul de IL-1β a fost mai mare în grupul tratat cu Rosuvastatină. Nivelele de IL-6 au avut o dispersie heterogenă în cadrul experimentului însă au fost înregistrate niveluri mai înalte în cadrul grupului septic netratat. Grupul tratat cu Simvastatină a avut nivele serice mai mari comparativ cu grupul tratat cu Rosuvastatină. Nivelele de TNF-α au fost mai mari pentru grupul septic netratat și cel tratat cu Rosuvastatină. Pentru grupul tratat cu Simvastatină nivelele TNF-α a fost similare cu cele din grupul control. Concluzii: Ambele statine au efecte anti-inflamatorii în cadrul acestui model de sepsis la șobolan indus prin tehnica ligaturării și puncției cecale. Dintre cele două, Simvastatina a avut un impact mai mare prin scăderea nivelelor circulante a unor markeri proinflamatori consacrați.

Background: Inflammation had a key role in several pathological conditions including atherosclerosis. Previous studies indicated that the proxisome proliferator-activated receptors (PPAR) are involved in numerous physiological and pathological conditions. The aim of this study was to investigate the effect of PPAR agonists including PPARα (fenofibrate), PPARβ/δ (GW0742), PPARγ (rosiglitazone) and pan PPAR (bezafibrate) administration on serum high-sensitive C-reactive protein (hsCRP) and interleukine-6 (IL-6) in male diabetic rats. Methods: The male Wistar rats were received streptozotocin for induction of type I diabetes. Then, they were randomly divided into five groups: diabetic, diabetic + fenofibrate (100 mg/kg/day; gavage), diabetic + GW0742 (1 mg/kg/day, subcutaneous), diabetic + rosiglitazone (8 mg/kg/day; gavage) and diabetic + bezafibrate (400mg/kg/day; gavage). After 21 days, the serum levels of hsCRP and IL-6 were measured using the enzyme-linked immunosorbent assay (ELISA) kits. Findings: Administration of different PPAR agonists did not alter serum hsCRP and IL-6 concentrations in diabetic animals. Conclusion: It seems that changes of serum inflammatory markers are not responsible for effects of PPARs agonist in atherosclerosis process and other mechanisms should be studied.

It was shown by the authors that changes of the level of cytokines reflected the degree of invasiveness of operative intervention. The endovideosurgical approach was less traumatic and provided a rapid rehabilitation of the patients in postoperative period. It is possible to consider the high levels of IL-10 as a predictor of development of local inflammatory process and as an indicator of probable infectious complications in postoperative period.

The roles of the immune system are recognized in the interaction between the host and the external environment, functionality and features dependent on a multitude of genetic and environmental factors. Specific and nonspecific immunity undergo a maturation throughout early childhood - crucial step in the further development of the organism. Cellular and molecular mechanisms are deciphering in the era of molecular medicine and their understanding is essential for effective therapeutic approach in pediatric pathology. [ABSTRACT FROM AUTHOR]

Introduction: Single Nucleotide Polymorphisms (SNPs) of IL 28 B and IL 10 were associated with sustained virological response (SVR) and liver fi brosis in chronic hepatitis C patients treated with peg-interferon (Peg IFN) and Ribavirin (RBV). Methods: We studied 188 patients with chronic hepatitis C who received antiviral therapy. RNA HCV was determined by RT-PCR and liver fi brosis was evaluated by transient elastography (Fibroscan) and serological tests (APRI score). The IL 28 B rs12979860 and IL 10 R -1087 (rs1800896) SNPs were genotyped using Custom Taqman SNP Genotyping Assays. Results: From 176 patients, 98 (55.68%) had SVR, 59 (33.52%) were nonresponders and 19 (10.80%) were relapsers. SVR was strongly associated with IL 28 B SNP genotypes (p<0.0005). Advanced/severe fi brosis was observed in 109 cases (57.97%). Fibrosis was not associated with IL 28 B SNP. IL 10 R SNP was a predictor for liver fi brosis: severe fi brosis was present in 66.67% of patients with GG genotype, 26.98% with GA and 51.02% with AA genotypes. The G allele of IL-10 SNP was associated with advanced fi brosis (OR: 2.40, p = 0.018). Conclusions: The determination of the interleukins polymorphisms is important in predicting the viral response to interferon therapy and evolution of liver fi brosis. [ABSTRACT FROM AUTHOR]

Copyright of HNO is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Hepatitis C virus (HCV) infection is one of the main causes of chronic liver disease worldwide, causing hepatic alterations, from minimal to extensive fibrosis and cirrhosis, with or without hepatocellular carcinoma (HCC). Genetic factors controlling the host immune response play a pivotal role in HCV infection, as cytokines are the predominant mechanisms implicated in host defense. The polymorphisms of IL-28B gene region determine the spontaneous and treatment induced clearance of genotype 1 HCV. Several findings demonstrated that some SNPs in the IL-28B gene are closely associated with pegylated-interferon/Ribavirin responsiveness. TNF-α and IL-10 secretion are involved in the inflammatory process caused by HCV infection. Also was suggested that the persistence of the virus and the response to antiviral therapy are associated with the production of inappropriate levels of TNF-α and its genetic polymorphisms -238 and -308. The predominance of IL-10 (-1082) GG genotype, associated with high IL-10 gene expression is frequently found in patients with spontaneous viral clearance. The chemokine Interferon-gamma Inducible protein 10 (IP-10, CXCL-10) is a promising single marker correlated with liver fibrosis, independent negative predictor of treatment outcome in HCV infected patients. Some studies showed a strong correlation between the grade of fibrosis and IL-6 polymorphisms (like IL-6 -174 G/C allele). Also patients that were non responders to treatment had higher levels of IL-8 compared with patients that responded. By predicting which persons are most likely to respond to IFN-based therapy, the examination of polymorphisms of these cytokines may help to manage an individualized approach to treat HCV patients. [ABSTRACT FROM AUTHOR]

The aims of this cross-sectional study were to explore the ability of serum interleukin 18 (IL-18) and adiponectin to identify metabolic syndrome (MetS), and to verify their association with an index of central lipid overaccumulation (lipid accumulation product (LAP)) and cardiometabolic risk factors in a population of middle-aged Brazilian men. A group of 218 apparently healthy middle-aged Brazilian men (age, 50.3 ± 4.97 years) underwent anthropometric, clinical, sociodemographic, and standard serum biochemical assessments. LAP was calculated and the study participants were categorized into 3 groups according to serum IL-18 and adiponectin cut-points tertiles to verify the association of these biomarkers with cardiometabolic risk factors. The MetS group had more less active ( p = 0.03) and obese ( p < 0.01) individuals who exhibited higher IL-18 ( p < 0.01) and lower adiponectin ( p < 0.01) than did those in the group with no MetS. After adjustments (age, smoking, alcohol consumption, physical activity level, and total body fat), serum IL-18 ≥ 336.4 pg/mL was an independent factor for MetS occurrence and it was directly associated with LAP (≥51.28), central obesity, hypertriglyceridemia, and hypertension ( p < 0.05), but not with high-density lipoprotein cholesterol (HDL-C). Serum adiponectin ≥ 7.02 μg/mL was negatively associated with MetS occurrence, LAP, hypertriglyceridemia, and low HDL-C ( p < 0.05), but not with central obesity and hypertension. In conclusion, both IL-18 and adiponectin demonstrated the ability to identify MetS in this population, with IL-18 being more accurate. The association of these biomamarkers with LAP and cardiometabolic risk factors highlights its relevance as a diagnostic tool. [ABSTRACT FROM AUTHOR]

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Copyright of Der Schmerz is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Inflammation had a key role in several pathological conditions including atherosclerosis. Previous studies indicated that the proxisome proliferator-activated receptors (PPAR) are involved in numerous physiological and pathological conditions. The aim of this study was to investigate the effect of PPAR agonists including PPARα (fenofibrate), PPARβ/δ (GW0742), PPARγ (rosiglitazone) and pan PPAR (bezafibrate) administration on serum high-sensitive C-reactive protein (hsCRP) and interleukine-6 (IL-6) in male diabetic rats. Methods: The male Wistar rats were received streptozotocin for induction of type I diabetes. Then, they were randomly divided into five groups: diabetic, diabetic + fenofibrate (100 mg/kg/day; gavage), diabetic + GW0742 (1 mg/kg/day, subcutaneous), diabetic + rosiglitazone (8 mg/kg/day; gavage) and diabetic + bezafibrate (400mg/kg/day; gavage). After 21 days, the serum levels of hsCRP and IL-6 were measured using the enzyme-linked immunosorbent assay (ELISA) kits. Findings: Administration of different PPAR agonists did not alter serum hsCRP and IL-6 concentrations in diabetic animals. Conclusion: It seems that changes of serum inflammatory markers are not responsible for effects of PPARs agonist in atherosclerosis process and other mechanisms should be studied. [ABSTRACT FROM AUTHOR]

Concurrent resistance and aerobic exercise (CE) is recommended to ageing populations, though is postulated to induce diminished acute molecular responses. Given that contraction-induced cytokine mRNA expression reportedly mediates remunerative postexercise molecular responses, it is necessary to determine whether cytokine mRNA expression may be diminished after CE. Eight middle-aged men (age, 53.3 ±1.8 years; body mass index, 29.4 ± 1.4 kg·m−2) randomly completed (balanced for completion order) 8 × 8 leg extensions at 70% maximal strength (RE), 40 min of cycling at 55% of peak aerobic workload (AE), or (workload-matched) 50% RE and 50% AE (CE). Muscle (vastus lateralis) was obtained pre-exercise, and at 1 h and 4 h postexercise, and analyzed for changes of glycogen concentration, tumor necrosis factor (TNF)α, TNF receptor-1 and -2 (TNF-R1 and TNF-R2, respectively), interleukin (IL)-6, IL-6R, IL-1β, and IL-1 receptor-antagonist (IL-1ra). All exercise modes upregulated cytokine mRNA expression at 1 h postexercise comparably (TNFα, TNF-R1, TNF-R2, IL-1β, IL-6) ( p < 0.05). Expression remained elevated at 4 h after RE and AE ( p < 0.05), though returned to pre-exercise levels after CE ( p > 0.05). Moreover, AE and RE upregulated IL-1β and IL-1ra expression, whereas CE upregulated IL-1β expression only ( p < 0.05). Only AE reduced muscle glycogen concentration ( p < 0.05), whilst upregulating receptor expression the greatest; though, IL-6R expression remained unchanged after all modes ( p > 0.05). In conclusion, in middle-aged men, all modes induced commensurate cytokine mRNA expression at 1 h postexercise; however, only CE resulted in ameliorated expression at 4 h postexercise. Whether the RE or AE components of CE are independently or cumulatively sufficient to upregulate cytokine responses, or whether they collectively inhibit cytokine mRNA expression, remains to be determined. [ABSTRACT FROM AUTHOR]

Purpose. To evaluate the serum levels of infl ammatory markers in children with alterations in nutritional status and the correlation of these markers with clinical diagnoses of infection. Methods. We conducted a prospective study on 120 children admitted to the Pediatric Clinic I Tg. Mures. We have followed the nutritional status and the presence or absence of infectious signs, the children being evaluated anthropometrically and by laboratory analysis (suggestive infection markers). Results. Underweight was found in 28.3% of children, and 24.2% were overweight. Clinically, at least one infectious syndrome has been identified in 31.7% of children, ESR being increased in these children compared to the healthy ones (p=0.034); no differences were observed in the other serological markers. We have found IL-6 and IL-8 values below the detection limit especially in underweight children with diagnosis of infection; significantly higher values of IL-6 and IL-8 were found in overweight children with a diagnosis of associated infection. Conclusions. Interleukins have significantly lower values in underweight children, even in the context of a possible infection. In order to confirm or infirm an infectious syndrome, the clinical judgment is not enough and the corroboration with complex laboratory data is necessary. [ABSTRACT FROM AUTHOR]

Physical exercise can improve health and may lead to changes in the functionality of the immune system. Moderate intensity exercise can reduce the risk of infection by shifting the overall immune response towards a T helper type 1 pattern. This study investigates the effect of 12 weeks of swimming on the cytokine profile of lymph node cells and macrophages and of the nitric oxide production by these cells. BALB/c mice were divided into 2 groups. The exercise group was subjected to swimming exercise. Lymph node cells culture showed that concentrations of interferon-γ and tumour necrosis factor-α were higher in the exercised group, while levels of interleukine-4 and interleukine- 10 were significantly decreased in this group. The interleukine-10/interferon-γ ratio tended towards a T helper type 1 profile. Moreover, macrophages isolated from exercised mice produced more interleukine-12 and tumour necrosis factor-α following lipopolysaccharide stimulus. Challenging these macrophages with Leishmania major resulted in higher interleukine- 12 production than was observed with macrophages from the control group. Nitric oxide production was increased in macrophages isolated from exercised group following lipopolysaccharide stimulus but not following infection with Leishmania major . These data suggest that exercise biases the immune system towards a T helper type 1 response profile. [ABSTRACT FROM AUTHOR]

The effect of duration-matched concurrent exercise training (CET) (50% resistance (RET) and 50% endurance (EET) training) on physiological training outcomes in untrained middle-aged men remains to be elucidated. Forty-seven men (age, 48.1 ± 6.8 years; body mass index, 30.4 ± 4.1 kg·m−2) were randomized into 12-weeks of EET (40-60 min of cycling), RET (10 exercises; 3-4 sets × 8-10 repetitions), CET (50% serial completion of RET and EET), or control condition. The following were determined: intervention-based changes in fitness and strength; abdominal visceral adipose tissue (VAT), total body fat (TB-FM) and fat-free (TB-FFM) mass; plasma cytokines (C-reactive protein (CRP), tumor necrosis factor-α (TNFα) interleukin-6 (IL-6)); muscle protein content of p110α and glucose transporter 4 (GLUT4); mRNA expression of GLUT4, peroxisome proliferator-activated receptor-γ coactivator-1α−β, cytochrome c oxidase, hexokinase II, citrate synthase; oral glucose tolerance; and estimated insulin sensitivity. CET promoted commensurate improvements of aerobic capacity and muscular strength and reduced VAT and TB-FM equivalently to EET and RET ( p < 0.05), yet only RET increased TB-FFM ( p < 0.05). Although TNFα and IL-6 were reduced after all training interventions ( p < 0.05), CRP remained unchanged ( p > 0.05). EET reduced area under the curve for glucose, insulin, and C-peptide, whilst CET and RET respectively reduced insulin and C-peptide, and C-peptide only ( p < 0.05). Notwithstanding increased insulin sensitivity index after all training interventions ( p < 0.05), no change presented for GLUT4 or p110α total protein, or chronic mRNA expression of the studied mitochondrial genes ( p > 0.05). In middle-aged men, 12 weeks of duration-matched CET promoted commensurate changes in fitness and strength, abdominal VAT, plasma cytokines and insulin sensitivity, and an equidistant glucose tolerance response to EET and RET; despite no change of measured muscle mechanisms associative to insulin action, glucose transport, and mitochondrial function. [ABSTRACT FROM AUTHOR]

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Summary: Objective: To examine the effect of the glycemic index (GI) of a pre-exercise (PRE-ex) meal on plasma cytokine responses and endurance performance when carbohydrate-electrolyte (CHO-E) drink was consumed during exercise. Methods: Eight endurance-trained male runners (age: 28.6±2.7 years; body mass: 61.9±1.71kg; : 58.5±1.6mlkg−1 min−1) completed three trials in a randomized order. The pre-exercise meal consisted of either high-GI (HGI) (GI=83), low-GI (LGI) foods (GI=36) or control (CON) (low energy sugar-free jelly) was given to the participant 2h before a 21-km performance run on a level treadmill. During each trial, 2mlkg−1 BM of 6.6% CHO-E solution was consumed immediately before exercise and every 2.5-km afterward. Blood samples were collected before (pre-meal), and 120min after ingestion the meal (120min), immediately (POST), and 60min (POST-60min) after exercise. Results: No difference was found in time to complete the 21-km run between LGI and HGI. The interleukin-6 (IL-6) level increased by more than 100 times immediately after exercise in the three trials and returned to the basal level only on LGI at POST-60min. In contrast, interleukin-2 (IL-2) level showed a transitory decrease at POST on CON (p <0.001). Glucose concentrations did not recover to the pre-meal level by POST-60min on HGI only. Cortisol concentrations increased throughout the exercise and were lower on LGI when compared with CON (p <0.05) at POST-60min. Conclusions: HGI and LGI demonstrated similar performance when CHO-E solution was consumed during a 21-km run. However, pre-exercise LGI meal attenuated the increases in cortisol and quickened the recovery of the increased IL-6 value. [Copyright &y& Elsevier]

We have cloned a cDNA sequence encoding the second bovine β-galactoside-α2,6-sialyltransferase whose sequence shares more than 75% of identity with hST6Gal II cDNA coding sequence. The bovine gene, located on BTA 11, spans over 50 kbp with five exons (E1–E5) containing the 1488 bp open reading frame and a 5′-untranslated exon (E0). The gene expression pattern reveals a specific tissue distribution (brain, lungs, spleen, salivary, and mammary glands) compared to ST6Gal I which is ubiquitously expressed. We identified for bovine ST6Gal II three kinds of transcripts which differ by their 5′-untranslated regions. Among them, two transcripts are brain specific whereas the third one is found in all of the tissues expressing the gene. Two pFlag-bST6Gal II vector constructions were separately transfected in COS-1 cells in order to express either membrane-bound or soluble active forms of ST6Gal II. Enzymatic assays with these two forms indicated that the enzyme used the LacdiNAc structure (GalNAcβ1,4GlcNAc) as a better acceptor substrate than the Type II (Galβ1-4GlcNAc) disaccharide. Moreover, the enzyme's efficiency is improved when the acceptor substrate is provided as a free oligosaccharide rather than as a protein-bound oligosaccharide. In order to investigate the potential role of ST6Gal II during the acute phase of inflammation, we used primary cultures of bovine mammary epithelial cells which were stimulated with pro-inflammatory cytokines. It appears that the ST6Gal II gene was upregulated in cells stimulated by IL-6. This result suggested that α2,6-sialylation mediated by this gene could contribute to organism's response to infections. [ABSTRACT FROM PUBLISHER]

The pathogenesis of gastric ulcer is associated with remodeling of extracellular matrix (ECM) by various matrix metalloproteinases (MMPs). However, how MMPs are regulated during nonsteroidal anti-inflammatory drug (NSAID)-induced acute gastric ulceration is not well studied. In this study, different NSAIDs (80 mg/kg b.w.) were applied to generate acute gastric ulcer in the BALB/c mouse and the regulation of MMPs were investigated. NSAIDs caused dose-dependent induction in MMP-9 and -3 activities and expressions in ulcerated gastric tissues along with significant infiltration of inflammatory cells and disruption of gastric mucosal layer. In addition, an increase in tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-8 expression, excessive generation of hydroxyl radical (•OH), and protein oxidation and lipid peroxidation were observed in acute ulcerated gastric tissues. In this study, the efficacy of melatonin on activities of MMP-9 and -3 during prevention of gastric ulcers was tested. Melatonin at a dose of 60 mg/kg b.w. downregulated MMP-9 and -3 both at the enzyme and protein levels in mouse gastric tissues during prevention as well as healing of acute gastric ulcers. It also blocked oxidative stress via inhibition of protein oxidation, lipid peroxidation, •OH generation and SOD-2 expression. Moreover, it suppressed myeloperoxidase activity and expressions of TNF-α, IL-1β and IL-8. This study documents for the first time that induction of MMP-9 and -3 activities accompany NSAID-induced inflammation and oxidative stress in gastric tissues and indicates that, melatonin may be a preventive or therapeutic remedy for gastric ulcers. [ABSTRACT FROM AUTHOR]

Fetal inflammatory response syndrome (FIRS) is caused by stimulation of the foetal immune system and biosynthesis of pro-inflammatory cytokines in the human foetus following intra uterine infection and/or premature membrane rupture. Several diagnostic features characterise FIRS during foetal life or at birth, including elevated levels of interleukin-6 in the cord blood, histological funiculitis or small foetal thymus size measured by ultrasound. A relationship between neonatal morbidity and foetal inflammation has been demonstrated by the increased concentration of IL-6 in cord blood or amniotic fluid in children who develop periventricular leukomalacia, bronchopulmonary dysplasia or cerebral palsy. Preventing adverse neonatal outcome associated with FIRS is a real challenge for neonatology. In at risk situations, such as premature rupture of membranes, maternal glucocorticoids, antibiotic therapy and the obstetric point of view (whether to continue with the pregnancy or extract the foetus) must be discussed. [ABSTRACT FROM AUTHOR]

The aim of the study was to investigate the therapeutic effect and mechanism of proanthocyanidins from grape seeds (GSPE) in the treatment of ulcerative colitis (UC). Rats were intragastrically administered different doses of GSPE (100, 200, and 400 mg/kg) per day for 7 days after UC was twice-induced by intracolonic injection of 2,4,6-trinitrobenzene sulfonic acid (TNBS)dissolved in 50% ethanol. Sulfasalazine (SASP) at 200 mg/kg was used as a positive control drug. Macroscopic and microscopic damage scores and changes in weight/length ratio (mg/mm) of colon segments were analyzed. The levels of malonyldialdehyde (MDA), interleukin (IL)-1β, IL-2, IL-4, and myeloperoxidase (MPO) activity in the colon tissues and MPO activity in the serum were all measured by biochemical methods or double antibody sandwich ELISA methods. Compared with the TNBS control group, GSPE treatment facilitated recovery of pathologic changes in the colon after insult with TNBS, as demonstrated by increased body weight (p < 0.01) and decreased colonic weight/length ratio (p < 0.01); GSPE also notably reduced the colonic macroscopic and microscopic damage scores (p < 0.01). The MPO activity in colon tissues and serum of rats treated with GSPE was significantly lower than that in the TNBS control group. The MDA and IL-1β levels of colon tissues were also decreased in GSPE groups. The intestinal antiinflammatory effect of GSPE was accompanied by a significant improvement of IL-2 and IL-4 levels in the colon tissues of rats in the high-dose GSPE group (p < 0.05). Compared with the SASP group, GSPE groups had no significant difference in the therapeutic effect (p > 0.05). GSPE exerts a beneficial antiinflammatory effect in the acute phase of TNBS-induced colitis in rats by downregulating some of the mediators involved in the intestinal inflammatory response, inhibiting inflammatory cell infiltration and antioxidation damage, promoting damaged tissue repair to improve colonic oxidative stress, decreasing production of proinflammatory cytokines IL-1β, and increasing production of antiinflammatory cytokines IL-2 and IL-4. Pour examiner l’effet thérapeutique et le mécanisme des proanthocyanidines extraites des graines de raisin (GSPE) chez des rats souffrant de colite ulcéreuse (CU) induite par l’acide 2,4,6-trinitrobenzène sulfonique (TNBS), on leu a administré différentes doses de GSPE (100, 200 et 400 mg/kg) par voie intragastrique, tous les jours pendant 7 jours, après que la CU a été induite deux fois par l’injection intracolique de TNBS dissous dans de l’éthanol 50 %. La sulfasalazine (200 mg/kg, SASP) a servi de médicament témoin positif. Puis les rats ont été sacrifiés. Les scores des lésions microscopiques et macroscopiques, et les modifications de la relation poids/longueur (mg/mm) des segments de côlon ont été analysés. Les taux de malonyldyaldéhyde (MDA), interleukine-1β (IL-1β), interleukine-2 (IL-2), interleukine-4 (IL-4) et l’activité de la myéloperoxydase (MPO) dans les tissus coliques ainsi que l’activité MPO dans le sérum ont tous été mesurés par des méthodes biochimiques et des tests ELISA sandwich. Comparativement a ce qui a été observé chez le groupe témoin TNBS, le traitement avec les GSPE a facilité la régression des modifications pathologiques induites par le TNBS, comme démontré par une augmentation de poids (p < 0,01), une diminution de la relation poids/longueur (p < 0,01) colique et une réduction considérable des scores microscopiques et macroscopiques du côlon (p < 0,01). L’activité MPO dans les tissus coliques et le sérum des rats traités avec les GSPE a été nettement plus faible que celle du groupe témoin TNBS. Les taux de MDA et d’IL-1β dans les tissus coliques ont aussi diminué chez les groupes GSPE. L’effet anti-inflammatoire intestinal des GSPE a été accompagné d’une augmentation significative des taux d’IL-2 et d’IL-4 dans les tissus coliques des rats du groupe GSPE 400 mg/kg (p < 0,05). Comparativement au groupe SASP, les groupes GSPE n’ont pas montré de différence significative dans l’effet thérapeutique (p > 0,05). Les GSPE ont un effet antiinflammatoire bénéfique dans la phase aiguë de la colite induite par le TNBS, en diminuant un certain nombre de médiateurs impliqués dans la réponse inflammatoire intestinale, en inhibant l’infiltration cellulaire inflammatoire, les dommages oxydatifs, en favorisant la réparation du tissu lésé pour diminuer le stress oxydatif colique, en diminuant la production des cytokines proinflammatoires IL-1β et en augmentant celle d [ABSTRACT FROM AUTHOR]

It is known that immune function decreases with age. There is the possibility that changes in the immune system to be a critical predisposing factor in the aging process; defining the immunological dysfunctionality in the elderly can add a new insight into the aging mechanisms. Getting older, there are alterations in the acquired immunity, especially in cells of the immune system T and B lymphocytes. Less scientifically proved are alterations in the innate immunity (dendritic cells, macrophages, polymorphonuclear leucocytes and complement) and in the mucosal immunity. [ABSTRACT FROM AUTHOR]

Abstract: Aim of this work: Aziridines have been shown to possess marked immunotropic activity. In this study, the in vitro effects of a new aziridine, 2-hydroxy-methyl-1-(N-phtaloyltryptophyl) aziridine, were determined on the proliferative responses of human lymphocytes stimulated by mitogens and on interleukin (IL-2, IL-6) secretion. Material and methods: Peripheral blood lymphocytes were isolated using differential centrifugation on a density gradient of Ficoll-Paque. They were cultured with or without mitogens (Concanavalin A and lipopolysaccharide), and with different concentrations of the aziridine. Proliferation was monitored by direct cell counts and confirmed by MTT [3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. After different incubations, IL-2 and IL-6 were determined by using commercially avaible Elisa kits. Results: The aziridine tested significantly stimulated the resting and mitogen T and B lymphocyte proliferation at concentrations between 1 μM and 1 mM, in a dose-dependent manner. It also increased IL-2 and IL-6 secretion. Conclusion: 2-hydroxy-methyl-1-(N-phtaloyltryptophyl) aziridine displayed immunomodulatory properties and is potentially immunostimulant. It could be used to provide non-specific cell-mediated immune responses. [Copyright &y& Elsevier]

The purpose of this study was to examine changes in serum cytokines after repeated bouts of aerobically biased eccentric exercise. Six untrained males ran down a –13.5% treadmill grade for 60 min on two occasions (RUN1 and RUN2) at a speed equal to 75% of their VO2 peak on a level grade; runs were spaced 14 d apart. Serum was collected before, after, and every hour for 12 h, and every 24 h for 6 d. Cytokines were assessed using 17 multiplex bead technology (Bio-Rad). Creatine kinase (CK) and delayed-onset muscle soreness (DOMS) were assessed before and 24–120 h after. Results were analyzed using a repeated measures analysis of variance (p ≤ 0.05). All comparisons were between RUN1 and RUN2. CK and DOMS were significantly elevated after RUN1 compared with RUN2, indicative of a repeated bout effect. Regarding cytokines, during the initial 12 h period after RUN2, there was a 50% decrease in pro-inflammatory interleukin-6 (IL-6), a 10% decrease in pro-inflammatory macrophage chemotactic protein-1, and a 95% elevation in anti-inflammatory interleukin-10 (IL-10). Regarding 24 h periods, after RUN2 there was an 8% reduction in pro-inflammatory interleukin-8 (IL-8). However, pro-inflammatory macrophage inflammatory factor-1β (MIF-1β) was 18% higher during the 12 h after RUN2. The overall cytokine profile suggests a slight reduction in systemic inflammation after RUN2. [ABSTRACT FROM AUTHOR]

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The pentacyclic triterpene maslinic acid (MA) is a natural compound present in the non glyceride fraction of pomace olive oil, also called orujo olive oil. This compound has previously demonstrated antioxidant properties against lipid peroxidation in vitro , but its effects on reactive oxygen and nitrogen-derived species and pro-inflammatory cytokines generated by a cell system have not yet been investigated. In this study, we have tested the effect of MA upon oxidative stress and cytokine production using peritoneal murine macrophages. MA significantly inhibited the enhanced production of nitric oxide (NO) induced by lypopolysaccharide (LPS) when it was measured by the nitrite production with an inhibitory concentration 50% value (IC 50 ) of 25.4 µM. This inhibiting effect seems to be consequence of an action at the level of the LPS-induction of the inducible nitric oxide synthethase (iNOS) gene enzyme expression rather than to a direct inhibitory action on enzyme activity. The secretion of the inflammatory cytokines interleukine-6 and TNF-a from LPS-stimulated murine macrophages was also significantly reduced ( p These results suggest a potential biopharmaceutical use of this hydroxy-pentacyclic triterpene derivative, present in orujo olive oil, on preventing oxidative stress and pro-inflammatory cytokine generation. [ABSTRACT FROM AUTHOR]

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