Ghorbanali Rahimian1, Mohammad Hosein Sanei2, Hedayatollah Shirzad3, Fatemeh Azadegan-Dehkordi4, Afshin Taghikhani1, Loghman Salimzadeh4, Morteza Hashemzadeh-Chaleshtori4, Mahmoud Rafieian-Kopaei5, Nader Bagheri6. 1. Department of Internal Medicine, Shahrekord University of Medical Sciences, Shahrekord, Iran. 2. Department of Pathology, Isfahan University of Medical Sciences, Isfahan, Iran. 3. Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. Electronic address: Shirzadeh@SKUMS.ac.ir. 4. Cellular and Molecular Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. 5. Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran. 6. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: n.bagheri1985@gmail.com.
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.
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-infectedpatients 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-infectedpatients 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.
Authors: Stephanie Y Owyang; Min Zhang; Mohamad El-Zaatari; Kathryn A Eaton; Shrinivas Bishu; Guoqing Hou; Helmut Grasberger; John Y Kao Journal: Helicobacter Date: 2020-10-06 Impact factor: 5.182