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Aim of the study: Few population-based studies have been conducted to report the prevalence of non-alcoholic fatty liver disease (NAFLD) and determine its risk factors in Iran, particularly in Shahrekord, southwest Iran. The main aim of this population-based, case-control study was to determine the prevalence of NAFLD and its potential risk factors in an Iranian population-based cohort study in Shahrekord, Iran. Material and methods: We compared 1153 cases with NAFLD at 35 to 70 years to 1153 frequency-matched NAFLD-free controls from a population-based Shahrekord cohort study. Data collection and assessed risk factors (demographics, anthropometrics, clinical and biochemical factors, and laboratory tests) were performed based on the Shahrekord cohort study protocol. Chi-square test, stepwise selection with backward likelihood ratio, logistic regression and log-binomial regression model with 95% confidence interval were performed to determine risk factors with significant effects on NAFLD. Results: In this study, the mean (± standard deviation) age of the participants was 50.23 (±8.70) years. The prevalence of NAFLD and metabolic syndrome with 95% confidence interval were 16.47% (15.61-17.36%) and 32.74% (30.83-34.70%), respectively. There was a significant difference in the frequency of waist circumstance, triglycerides, body mass index, blood pressure, and alanine aminotransferase between cases and controls (p < 0.001). According to log-binomial model results, socioeconomic status, hypertension, diabetes, and physical activity were significantly associated with NAFLD. Conclusions: Our findings have important clinical and public health implications in southwest Iran for monitoring the prevalence of NAFLD and important risk factors to manage, screen, prevent, and reduce NAFLD and related factors. [ABSTRACT FROM AUTHOR]

Background: Ulcerative colitis (UC) is a chronic inflammatory disorder of the large intestine histologically characterized by indistinct sustained inflammatory responses. Genetical susceptibility and environmental factors’ effects play the roles in disease occurrence and it can be life threatening if remains untreated. It seems that intensification of inflammatory responses in this condition is not restricted to a specific cell line of T lymphocytes. Our aim was to determine the number of T helper 9 (Th9) cells in inflamed colonic biopsies of UC patients. We also correlated it with interleukin (IL)-9 protein level in addition to certain genes expressions associated with Th9 phenotype. Methods: Expression of CD4 and IL-9 were evaluated by immunohistochemical staining. Enzyme linked immunosorbent assay (ELISA) was performed to determine the colonic expression of IL-9 protein and finally mRNA expressions of interferon regulatory factor 4 (Irf4), Smad2, and Smad3 were measured by real-time polymerase chain reaction (RT-PCR) as critical transcription factors of Th9 differentiation. Results: Number of Th9 cells was significantly increased in inflamed samples as compared with normal tissues. Also quantitative measurement of IL-9 by ELISA and mRNA expressions of Irf4, Smad2, and Smad3 showed notable correlative enhancements in patient’s samples. Conclusion: Function and number of Th9 cells are up-regulated in the inflamed mucosa of UC patients as with the protein secretion of IL-9 and mRNA expressions of Irf4, Smad2, and Smad3, so Th9 cells and IL-9 may become remarkable therapeutic targets for IBD treatment in the future. [ABSTRACT FROM AUTHOR]

Helicobacter pylori(H. pylori) infection has been involved in the pathogenesis of most important gastroduodenal diseases. Matrix metalloproteinases (MMPs) are a large family of zincendopeptidases which play important roles in degradation of extracellular matrix (ECM) and various inflammatory diseases. Therefore, we examined MMP-7 mRNA levels in the gastric mucosa of patients withH. pyloriinfection and evaluated the effects of virulence factors, such asvacA(vacuolating cytotoxin A) andcagA(cytotoxin-associated gene), inH. pylori-infected patients upon the MMP-7 mRNA mucosal levels. We also determined the correlation between mucosal MMP-7 mRNA levels and the types of disease. Total RNA was extracted from gastric biopsies of 50H. pylori-infected patients and 50 uninfected individuals. Mucosal MMP-7 mRNA expression level inH. pylori-infected and non-infected gastric biopsies was determined by real-time polymerase chain reaction (PCR). The presences of cagA and vacA virulence factors was evaluated using PCR. MMP-7 expression was significantly higher in biopsies of patients infected withH .pyloricompared to uninfected individuals. In addition, mucosal MMP-7 mRNA expression inH. pylori-infected patients significantly associated with thecagAstatus and the types of disease. Our results suggest that MMP-7 might be involved in the pathogenesis ofH. pylori. Peptic ulcer was associated withcagpathogenicity island-dependent MMP-7 upregulation. [ABSTRACT FROM AUTHOR]

Helicobacter pylori(H. pylori) is associated with gastric ulcer and gastric adenocarcinoma. Polymorphisms in the host genes coding for Toll-like receptors (TLRs) may influence the innate and adaptive immune response to the infection, affecting the susceptibility toH. pylorior the disease outcomes. However, the details and association with different polymorphism and clinical expression of infection remain unclear. A case-control study consisting of 58 patients withH. pyloriinfection and 44H. pyloriuninfection was conducted. Genomic DNA was extracted and genotypes of TLR4 Asp299Gly polymorphism were assessed through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Mucosal cytokines expression inH. pylori-infected and uninfected gastric biopsies was determined by real-time PCR. The expression of IL-6, IL-17, IL-21, IL-23 and TGF-β1 was significantly higher in patients with D299G polymorphism in TLR4. But the expression of IL-18 between patients with single-nucleotide polymorphisms (SNPs) in TLR4 and patients with the wild-type allele was not significant. InH. pylori-infected patients with gastritis, SNPs in TLR4 may alter cytokine expression toward Th17 immune response in the gastric mucosa and may have increased risk for the development of peptic ulcer. [ABSTRACT FROM AUTHOR]

Helicobacter pylori (H. pylori) infection is generally acquired during early childhood; therefore, the immune response which usually takes place at this age may influence or even determine susceptibility to the infection contributing to the clinical outcomes in adulthood. Several cytokines including IL-6, IL-10, and TGF-β1 as well as Foxp3(+) cell numbers have been shown to be higher; however, some other cytokines consisting of IL-1β, IL-17A, and IL-23 are lower in infected children than in infected adults. Immune response to H. pylori infection in children is predominant Treg instead of Th17 cell response. These results indicate that immune system responses probably play a role in persistent H. pylori infection. Childhood H. pylori infection is also associated with significantly lower levels of inflammation and ulceration compared with adults. This review, therefore, aimed to provide critical findings of the available literature about comparative immune system in children and adults with H. pylori infection. [ABSTRACT FROM AUTHOR]

Background: Different therapeutic regimens were used for eradication of Helicobacter pylori, based on the cost, effectiveness and patient's compliance. The aim of this study was the evaluation of licorice compared with bismuth in quadruple regimen on eradication of H. pylori in patients with peptic ulcer disease (PUD). Materials and Methods: In a double.blind clinical trial study, 60 patients with PUD and positive rapid urease test were enrolled. The patients were randomly allocated into two equal groups. In first group, licorice, amoxicillin, metronidazole and omeprazole and in the second (control) group, bismuth subsalicylate, amoxicillin, metronidazole and omeprazole were prescribed respectively, and 4 weeks after treatment, in order to evaluate H. pylori eradication, urea breath test was done in all patients. The outcome of the study was the preference usage of licorice as an effective medication for H. pylori eradication. Results: Mean age of the patients in the control and case groups were 40.8±15.5 and 42.2±15.8 years, respectively (P = 0.726). Seventeen (56.7%) patients in control group and 16 (53.3%) in the case group were female (P = 0.795). Both groups were similar based on frequency of gastric or duodenal ulcer. Response to treatment were seen in 20 (67%) and 17 (57%) patients of case and control groups, respectively (P > 0.05). Conclusion: Our study showed that licorice is as effective as bismuth in H. pylori eradication; therefore, in patients whom bismuth is contraindicated, licorice can be used safely instead. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Helicobacter pylori (H. pylori) infection is the main cause of gastric inflammation. Regulatory T cells (Treg cells) suppress the activation and proliferation of antigen-specific T cells and mediate immunologic tolerance. TGF-β1 was shown to be secreted in a subset of Treg cells known as ‘Th3 cells’. These cells have not been sufficiently studied in context to H. pylori-induced inflammation in human gastric mucosa. In this study we therefore, aimed to investigate the expression of TGF-β1 in the context of H. pylori colonization in chronic gastritis, to examine the relationship between it and histopathologic findings and to compare it with virulence factors. Patients and methods: Total RNA was extracted from gastric biopsies of 48 H. pylori-infected patients and 38 H. pylori-negative patients with gastritis. Mucosal TGF-β1 mRNA expression in H. pylori-infected and uninfected gastric biopsies was determined by real-time PCR. Presence of vacA, cagA, iceA, babA2 and oipA virulence factors was evaluated using PCR. Results: TGF-β1 mRNA expression was significantly increased in biopsies of H. pylori-infected patients compared to H. pylori-uninfected patients. There was association between virulence factors and TGF-β1 mRNA expression. TGF-β1 mRNA expression in mucosa was significantly higher in patients with vacA s1 and s1m1. Conclusions: TGF-β1 may play an important role in the inflammatory response and promote the chronic and persistent inflammatory changes in the gastric. This may ultimately influence the outcome of H. pylori-associated diseases that arise within the context of gastritis and vacA may suffice to induce expression of TGF-β1 mRNA. [Copyright &y& Elsevier]

Background: This study assessed the effects of hypnotherapy in conjunction with pharmacotherapy versus pharmacotherapy on the quality of life in patients diagnosed with irritable bowel syndrome (IBS). Materials and Methods: This clinical trial used the convenience sampling method to enroll 34 IBS patients. Patients were selected according to Rome III criteria and divided into two groups: i) hypnotherapy plusstandard medical treatmentand ii) standard medical treatment. The QOL-IBS scale assessed patient quality of life at baseline, post-treatment and at the six month follow-up. Data were analyzed using analysis of covariance (ANCOVA). Results: There were significant differences observed between both groups at the post-treatment and follow-up stages in terms of quality of life (p<0.05). Conclusion: Standard medical treatment in addition to hypnotherapy can be used to improve quality of life in IBS patients. [ABSTRACT FROM AUTHOR]

Background: Fra-1 (fosl1) belongs to the activator protein1 (AP-1) family inducing IL-11 expression in oxidative stress condition. IL-11 plays a pivotal role in protecting epithelial barriers integrity. In this study, we investigated the Fra-1 gene expression in the inflamed mucosa of patients with ulcerative colitis (UC) as well as its relation to IL-11 expression. Materials and methods: We enrolled 20 patients and 20 healthy controls with definite UC based on the clinical criteria. Fra-1 gene expression in inflamed and non-inflamed colonic biopsies was determined by real-time polymerase chain reaction (RT-PCR). The IL-11 protein concentration was measured by Enzyme-Linked Immunosorbent Assay (ELISA) method. Pearson correlation was applied to calculate the relation between Fra-1 and IL-11. Results: An increased level of Fra-1 gene expression was observed in patients with mild ulcerative colitis. The protein concentration of IL-11 was also increased in mild UC patients. Conversely, a significant decrease of IL-11 protein level was detected in severe UC patients compared to control group. Conclusion: Oxidative stress in inflamed intestinal biopsies can induce fra-1 gene expression. Our findings suggest that Fra-1 transcription factor leads to the production of IL-11 protein in UC patients. [ABSTRACT FROM AUTHOR]

Introduction: Helicobacter pylori (H.pylori) infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells that contribute to sustain and expand the local inflammation. In this study, we sought to examine IL-1β expression in the H.pylori-infected and uninfected gastric mucosa and to elucidate the implication in the pathogenesis of H.pyloriassociated gastritis in humans. Methods: Total RNA was extracted from gastric biopsies of 80 H.pylori-infected patients and 45 H. pylori-negative patients. Mucosal IL-1β mRNA expression level in H.pyloriinfected and non-infected gastric biopsies was determined by real-time PCR. Results: IL-1β mRNA expression was significantly increased in biopsies of H.pylori-infected patients compared to H.pylori-negative patients. Conclusion: Mucosal IL-1β expression level is increased in patients with H.pylori infection. Therefore, we believe that IL-1β might be involved in the pathogenesis of H.pylori infection. [ABSTRACT FROM AUTHOR]

Helicobacter pylori ( H. pylori ) colonization induces vigorous innate and specific immune responses; however, the infection does not disappear and a chronic active gastritis continues if left untreated. It has been shown that the topographical pattern and immune response of gastritis are the main reasons for the bacteria persistence and the clinical outcome. Gastritis due to H. pylori is caused by a complicated interaction among a variety of T cell subsets. Regulatory T (Treg) cells suppressing the immune response of antigen-specific T-cells have recently been demonstrated to play a key role in chronic inflammation by immunologic tolerance. Treg cells have been identified as the major regulatory component of the adaptive immune response and being involved in H. pylori -related inflammation and bacterial persistence. There have been many controversies over the role of Treg cells in H. pylori infection. Many studies have shown that the local Treg response protects the gastric mucosa from intensified inflammation and tissue damage, and the risk of H. pylori -associated diseases has an inverse correlation with Treg accumulation, even if the decrease in the inflammatory response is recognized by Treg it causes increase in bacterial density. This paper reviews the role of Treg in different clinical expressions of H. pylori infection. [ABSTRACT FROM AUTHOR]

Abstract: Background: Helicobacter pylori (Hp) infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells that contribute to sustain and expand the local inflammation. Different clinical expressions of the infection may reflect distinctive patterns of cytokine expression. IL-1β, TNF-α, IL-17 and IL-23 have been reported to be involved in Hp-induced gastric mucosal inflammation, but the details and association to different patterns of inflammation and virulence factors remain unclear. Methods: Total RNA was extracted from gastric biopsies of 51 Hp-infected patients and 44 Hp-negative patients. Mucosal IL-18 mRNA expression in gastric biopsies was determined by Real-Time PCR. Presence of virulence factors was evaluated using PCR. Results: IL-18 mRNA expression was significantly increased in biopsies of Hp-infected patients compared to Hp-uninfected individuals. There was no association between virulence factors and IL-18 mRNA expression. Also severity of mononuclear infiltration was significantly higher in gastritis patients with vacA (m1)-positive compare patients with vacA (m2)-positive. Conclusions: IL-18 may play an important role in the inflammatory response and promote the chronic and persistent inflammatory changes in the stomach. This may ultimately influence the outcome of Hp-associated diseases that arise within the context of gastritis. [Copyright &y& Elsevier]

Peptic ulcer disease (PUD) is a common disease worldwide moreover known as stomach ulcer or peptic ulcer. Increased the number of T CD4+ helper cells in response to gastric infection by Helicobacter pylori (H. pylori) play an important role in the development of PUD. The aim of this study was to determine the frequency of T-bet+ cells in H. pylori -infection, its interaction with Th17/Treg cells and its association with the clinical consequences of the infection. A total of 63 patients with PUD, 89 patients with gastritis and 48 H. pylori -negative subjects were enrolled in this study. The number of T-bet+ cells were determined by immunohistochemistry. The numbers of T-bet+ cells and INF-γ expression in infected patients were significantly higher than uninfected. Moreover, the number of T-bet+ cells and INF-γ expression in infected patients with PUD were significantly higher than infected patients with gastritis. Additionally, the number of T-bet+ cells and INF-γ expression were found to be inversely correlated with degree of H. pylori density and chronic inflammation score (CIS) in infected patients with gastritis disease, but this correlation was positive in the infected patients with PUD. The number of T-bet+ cells was found to be positively correlated with the number of Th17 cells and inversely correlated with the number of Treg cells in infected patients with gastritis and PUD. Abnormal hyper-activation of T-bet+ cells during H. pylori -infection may lead to tissue damage caused by immunopathologic reactions. [ABSTRACT FROM AUTHOR]

Background Reactive oxygen species (ROS) is one of the pathogenic factors responsible for intestinal injury in Ulcerative colitis (UC). Nuclear factor erythroid-2 related factor 2 (Nrf2) plays a critical role against ROS factors to conserve epithelial integrity. This study aimed to localize Nrf2 and IL-17A protein in the inflamed mucosa of patients with ulcerative colitis. The gene expression of Nrf2 was also correlated with GST-A4 and PRDX1. Materials and methods A total of 20 patients and 20 healthy controls with definite UC based on the clinical criteria were enrolled for this study. The expression pattern of Nrf2 and IL-17A protein was compared in inflamed and non-inflamed colonic biopsies by immunohistochemical staining. Nrf2 , GST-A4 and PRDX1 gene expression were determined by real-time polymerase chain reaction (RT-PCR). Results In inflamed colonic biopsies, an increased level of Nrf2 protein factor was detected in epithelial cells. Conversely, IL-17A protein was presented more in mononuclear cells in mucosa and lamina propria regions. A significant increase of Nrf2 , GST-A4 gene expression was observed in both mild and severe patients with ulcerative colitis. GST-A4 gene expression indicated a high exponential rate in logistic regression. Conclusion Oxidative stress in inflamed colonic tissue can induce Nrf2 gene expression. The performance of Nrf2 transcription factor may lead to the induction of GST-A4 and PRDX1. IL-17A is less detected in intestinal inflammation, presenting Nrf2 factor. The present findings suggest that Nrf2 function in the gut plays a role in arresting both inflammatory response and oxidative damages of UC. [ABSTRACT FROM AUTHOR]

Background During Helicobacter pylori ( H. pylori ) infection CD4 + T cells in the gastric lamina propria are hyporesponsive and polarized by Th1/Th17 cell responses controlled by Treg cells. The objective of this study was to determine the number of Th17 cells in gastric mucosa of patients with gastritis and peptic ulcer and determined the relationship between main virulence factor of H. pylori and Th17 cells. Methods and materials A total of 89 H. pylori -infected gastritis patients, 63 H. pylori -infected peptic ulcer patients and 48 H. pylori -negative non-ulcer dysplasia patients were enrolled in this study. The number of Th17 was determined by immunohistochemistry. IL-8 and IL-17A expressions were determined by real-time polymerase chain reaction (qPCR). Also, the grade of chronic and active inflammation was investigated for involvement according to the density of neutrophils and mononuclear in gastric mucosal crypts, from one to all crypts. Results The number of Th17 cells and the expression of IL-8 and IL-17A in infected patients were significantly higher than uninfected subjects. The number of Th17 cells and the expression of IL-8 and IL-17A in infected patients with peptic ulcer were significantly higher than patients with gastritis. Additionally, the numbers of Th17 cells as well as the expression of IL-8 and IL-17A were positively correlated with the degree of H. pylori density in infected patients with peptic ulcer, while this correlation was negative in infected patients with gastritis. The numbers of Th17 cells as well as the expression of IL-8 and IL-17A were positively correlated with the degree of chronic inflammation. Conclusion The predominant Th17 cell responses may play a role in the pathogenesis of peptic ulcers disease in infected patients. [ABSTRACT FROM AUTHOR]

The outcome of Helicobacter pylori infection has been related to specific virulence-associated bacterial genotypes. The vacuolating cytotoxin (vacA), cagA gene, oipA and babA2 gene are important virulence factor involving gastric diseases. The objective of this study was to assess the relationship between virulence factors of H. pylori and histopathological findings. Material and methods Gastroduodenoscopy was performed in 436 dyspeptic patients. Antrum biopsy was obtained for detection of H. pylori , virulence factors and for histopathological assessment. The polymerase chain reaction was used to detect virulence factors of H. pylori using specific primers. Results vacA genotypes in patients infected with H. pylori were associated with cagA, iceA1 and iceA2. In the patients with H. pylori infection there was a significant relationship between cagA positivity and neutrophil activity ( P = 0.004) and chronic inflammation ( P = 0.013) and with H. pylori density ( P = 0.034). Neutrophil infiltration was found to be more severe in the s1 group than in the s2 group ( P = 0.042). Also was a significant relationship between oipA positivity and neutrophil activity ( P = 0.004) and with H. pylori density ( P = 0.018). No significant relationships were observed between other vacA genotypes and histopathological parameters. Conclusion H. pylori strains showing cagA, vacA s1 and oipA positivity are associated with more severe gastritis in some histological features but virulence factors of H. pylori do not appear to determine the overall pattern of gastritis. [ABSTRACT FROM AUTHOR]

Helicobacter pylori (H. pylori) infection is associated with gastritis and marked infiltration of the gastric mucosa by several cytokines secreting inflammatory cells. Different clinical forms of the infection may reflect distinctive patterns of cytokine expression. Interleukin (IL)-17, IL-21, IL-22, and IL-23 have been reported to be involved in H. pylori-induced gastric mucosal inflammation, but the details and relationship to different patterns of inflammation and virulence factors remain unclear. The present study was launched to analyse IL-6 expression in H. pylori-infected and uninfected gastric patients and to investigate its correlation with chronic gastritis among H. pylori-infected patients. Total RNA was extracted from the gastric antrum biopsies of 48 H. pylori-infected patients and 38 H. pylori uninfected patients. Mucosal IL-21 mRNA expression level in H. pylori-infected and uninfected gastric biopsy was determined by real-time PCR. The presence of vacA (vacuolating cytotoxin A) and cagA (cytotoxin associated gene A) virulence factors were evaluated using PCR. Interleukin- 21 mRNA expression was significantly high in biopsies of H. pylori-infected patients compared to H. pylori uninfected patients, and the mucosal IL-21 mRNA level was positively correlated with the grade of chronic inflammation. There was no association between virulence factors and IL-21 mRNA expression. We believe that IL-21 might be involved in the pathogenesis of H. pylori and might be an index of the severity of chronic gastritis. [ABSTRACT FROM AUTHOR]

B lymphocytes are primarily well known for their contribution to immunity by antibody production, antigen presentation and, the production of cytokines. In recent years several studies demonstrated the existence of B cells with regulatory functions, which have been termed regulatory B cells (B regs), similar to regulatory T cells (T regs). B regs are a subpopulation of B cells that have immunosuppressive effects via the production of regulatory cytokines including interleukin-10 (IL-10), transforming growth factor-β (TGF-β), and IL-35. B regs limit host defense against various pathogens. In addition, B regs contribute to increased levels of regulatory cytokines and leads to an induction of suppressive T regs , which exert broader suppressive functions against various pathogens. The high percentage of B regs is positively associated with viral and bacterial load and can contribute to poor vaccine responses. B regs can also facilitate pathogen survival at an early stage of infection, and subsequently cause increased severity of disease by inhibiting pro-inflammatory cytokine production, macrophage activation, and inflammatory T cells activation such as Th1, Th17, and Th22. Also, B regs afford protection against the hyper-inflammatory response in parasitic infections. Here we review the central role of B regs in many major bacterial and viral human infections, and provide an overview of the immunoregulatory mechanisms used by B regs. • Regulatory B cells (Bregs) are a subpopulation of B cells that have immunosuppressive effects. • The defective function of Bregs can lead to a dysregulated innate and adaptive immune responses. • B regs contribute to increased regulatory cytokines and leads to the induction of T regs. • B regs is associated with viral and bacterial load and can contribute to poor vaccine responses. • B regs can facilitate pathogen survival and cause increased severity of disease. [ABSTRACT FROM AUTHOR]