The role of T helper 1-cell response in Helicobacter pylori-infection

Helicobacter pylori (H. pylori) is a human pathogen affecting over 50% of the world population. This pathogen is usually associated with chronic inflammation of the gastric mucosa that can lead to peptic ulcer disease (PUD) and gastric cancer (GC), especially in susceptible individuals. These outcomes have been attributed to the interaction of several factors, including host genetic susceptibility, local innate and adaptive immune responses, virulence factors of H. pylori, and environmental factors. T helper (Th) cell subsets and their signature cytokines especially IFN-γ, contribute to anti-bacterial response, but at the mean time sustaining chronic inflammatory responses in the site of infection. It has been acknowledged that H. pylori-infection results in a Th1-dominant response and that inflammation of the gastric mucosa depends mainly on Th1 cell responses. But, the mechanism of the role of Th1 cell responses in H. pylori-infection has not yet been clearly explained. In this review, we will focus on the role of Th1 involved in H. pylori-infection, its interaction with Th17/Treg cells and its association with the clinical consequences of the infection

The role of Th1 and Th17 cells in glomerulonephritis.

CONTEXT T helper (Th) cells as an important part of the immune is responsible for elimination of invading pathogens. But, if Th cell responses are not regulated effectively, the autoimmune diseases might develop. The Th17 subset usually produces interleukin-17A which in experimental models of organ-specific autoimmune inflammation is very important. EVIDENCE ACQUISITIONS Directory of open access journals (DOAJ), Google Scholar, Embase, Scopus, PubMed and Web of Science have been searched. RESULTS Fifty-six articles were found and searched. In the present review article, we tried to summarize the recently published data about characteristics and role of Th1 and Th17 cells and discuss in detail, the potential role of these T helpers immune responses in renal inflammation and renal injury, focusing on glomerulonephritis. Published papers in animal and human studies indicated that autoimmune diseases such as rheumatoid arthritis and multiple sclerosis, classically believed to be Th1-mediated, are mainly derived from a Th17 immune response. Identification of the Th17 subgroup has explained seemingly paradoxical observations and improved our understanding of immune-mediated inflammatory responses. CONCLUSIONS Secretion of IL-17A, as well as IL-17F, IL-21, IL-22, suggests that Th17 subset may play a crucial role as a pleiotropic pro-inflammatory Th subset. There is experimental evidence to support the notion that Th1 and Th17 cells contribute to kidney injury in renal inflammatory diseases like glomerulonephritis

Inhibition of Th1 and Th17 Cells by Medicinal Plants and Their Derivatives: A Systematic Review.

Searching for new natural drugs that are capable of targeting Th1 and Th17 may lead to development of more effective treatments for inflammatory and autoimmune diseases. Most of the natural drugs can be derived from plants that are used in traditional medicine and folk medicine. The aim of this systematic review is to identify and introduce plants or plant derivatives that are effective on inflammatory diseases by inhibiting Th1 and Th17 responses. To achieve this purpose, the search terms herb, herbal medicine, herbal drug, medicinal plant, phytochemical, traditional Chinese medicine, Ayurvedic medicine, natural compound, inflammation, inflammatory diseases, Th1, Th17, T helper 1 or T helper 17 were used separately in Title/Keywords/Abstract in Web of Science and PubMed databases. In articles investigating the effect of the medicinal plants and their derivatives in inhibiting Th1 and Th17 cells, the effects of eight extracts of the medicinal plants, 21 plant-based compounds and some of their derivatives, and eight drugs derived from the medicinal plants' compounds in inhibiting Th1 and Th17 cells were reviewed. The results showed that medicinal plants and their derivates are able to suppress Th17 and Th1 T cell functions as well as cytokine secretion and differentiation. The results can be used to produce herbal drugs that suppress Th, especially Th17, responses. Copyright © 2017 John Wiley & Sons, Ltd

Correlation between expression levels of mRNA IL-6 and H. pylori-infected patients with cagA

BACKGROUND AND OBJECTIVE: Helicobacter pylori (H. pylori) infection is associated with marked infiltration inflammatory cells such as neutrophil, macrophage and H. pylori-specific T and B cell in the gastric mucosa. The molecular pathways that control H. pylori-associated inflammatory reaction are complex, but locally induced cytokines seem to contribute to maintaining the ongoing inflammation. The purpose of this study was to evaluate IL-6 gene expression in the H. pylori-infected and uninfected gastric patients and correlation it’s with cagA among H. pylori infected patients. METHODS: This study is case - control. Biopsies were collected from 58 H. pylori-infected patients and 44 uninfected. Mucosal IL-6 mRNA levels were measured by real-time PCR. Presence of cagA virulence factor was evaluated using PCR. Cytokine expression is presented as means and differences between infected and non-infected groups were analysed using the T-Test test. FINDINGS: The IL-6 mRNA expression levels were significantly more elevated in H. pylori-positive patients than uninfected. There was no association between cagA virulence factor in H. pylori-infected patients and IL-6 mRNA expression. Conclusion: The enhanced induction of IL-6 may be independent cagA virulence factor involved in the pathogenesis of H. pylori-associated gastritis

Genotyping of Hepatitis B Virus in HBsAg Positive Individuals Referred to the Health Centers of Shahrekord, Iran

Background & aim: Hepatitis B Virus is one of the most important viral hepatitis which includes eight genotypes based on genetic variations in the gene encoding virus RNA polymerase. Clinical picture, treatment response and prognosis of HBV infection is genotype dependent. Therefore, this study was aimed to determine the HBV genotypes in HBsAg-positive individuals. . Methods: This experimental study was conducted on one hundred and sixteen HBsAgpositiveindividuals referred to the health centers of Shahrekord, Iran, in 2011. Firstly, the viral nucleic acid was extracted from serum samples and subsequently, the samples were subjected to Polymerase Chain Reaction (PCR). Finally, genotyping was carried out on the positive samples, using Real-time PCR with type specific primers and probes. The data were analyzed using the chisquare test. Results: 23 out of 116 (19.8%) of the HBsAg-positive individuals were positive for HBV DNA. 17 out of 23 (73.9%) and 6 out of 23 (26.1%) of the patients were found to be infected with HBV genotypes of D and C, respectively. Conclusion: Same as other regions of Iran, genotype D, , is the dominate genotype of HBV in Shahrekord, Iran. However, genotype C may be one of the other common genotypes in this region

Role of Regulatory T-cells in Different Clinical Expressions of Helicobacter pylori Infection

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. © 2016 IMS

Association Between Helicobacter pylori cagA, babA2 Virulence Factors and Gastric Mucosal Interleukin-33 mRNA Expression and Clinical Outcomes in Dyspeptic Patients

Helicobacter pylori (H. pylori) infection has been reported in more than half of the world human population. It is associated with gastric inflammation and noticeable infiltration of the immune cells to the stomach mucosa by several cytokines secretion. IL-1 beta, IL-18 have been shown to contribute to H. pylori induced gastritis, but the details of inflammation and association of virulence factors remain unclear. IL-1 cytokine family has a new additional cytokine, Interleukin-33 (IL-33), which is contemplated to have an important role for host defense against microorganisms. H. pylori virulence factors important in gastritis risk are the cag pathogenicity island (cag-PAI) and babA. This study evaluated IL-33 mucosal mRNA expression levels in infected and uninfected patients and its relationship with bacterial virulence factors cagA, babA(2) and type of gastritis. Total RNA was extracted from gastric biopsies of 79 H. pylori-infected patients and 51 H. pylori-negative patients. Mucosal IL-33 mRNA expression levels in gastric biopsies were assessed using real-time PCR. Existence of virulence factors were detected by PCR. IL-33 mRNA expression was significantly higher in biopsies of H. pylori-infected patients compared to H. pylori-uninfected patients (P< 0.0001). Also there was a direct relationship between virulence factor bab-A2 and enhancement in IL-33 mRNA expression. Furthermore, IL-33 mRNA expression level was significantly lower in chronic gastritis patients compared with patients with active gastritis (P< 0.001). IL-33 may play a crucial role in the inflammatory response and induction of the chronic gastritis and severity of inflammatory changes in the gastric mucosa