We have located links that may give you full text access.
Journal Article
Research Support, Non-U.S. Gov't
Helicobacter pylori Colonization Protects Against Chronic Experimental Colitis by Regulating Th17/Treg Balance.
Inflammatory Bowel Diseases 2018 June 9
Background: Epidemiological studies have demonstrated an inverse association between Helicobacter pylori infection and the risk of developing inflammatory bowel disease (IBD). The mechanisms by which H. pylori infection protects against IBD are unclear. Here, we explored the possible protective effects and mechanisms of gastric H. pylori colonization on a chronic colitis model, with focus on whether H. pylori exerted its effects through regulating Th17/Treg immune responses.
Methods: Chronic colitis was induced by dextran sulfate sodium (DSS) treatment. Flow cytometry analysis was performed to determine Th17 cells, Treg cells, and M1/M2 macrophages in the spleen, mesenteric lymph nodes, and colonic lamina propria. The levels of Th17- and Treg-associated cytokines were measured by quantitative polymerase chain reaction. The direct effect of H. pylori extract on the polarization status of macrophages was determined in vitro.
Results: Gastric H. pylori colonization significantly ameliorated the severity of chronic DSS-induced colitis. H. pylori colonization decreased Th17 cells and mRNA levels of IL-17A, IL-17F, and IL-21 in the colon. Simultaneously, H. pylori colonization increased Treg cells and IL-10 expression. As to cytokines driving Th17 and Treg differentiation, H. pylori colonization increased TGFβ and decreased IL-6 and IL-23. Moreover, H. pylori colonization significantly increased M2 macrophages in the colon. In vitro, H. pylori extract promotion of M2 macrophage polarization was dependent on the presence of CagA.
Conclusions: H. pylori colonization protects against chronic DSS-induced colitis via balancing Th17/Treg responses and shifting macrophages toward anti-inflammatory M2 phenotype. Our results strengthen the rationale for gastric H. pylori colonization affecting the immune homeostasis of the colon.
Methods: Chronic colitis was induced by dextran sulfate sodium (DSS) treatment. Flow cytometry analysis was performed to determine Th17 cells, Treg cells, and M1/M2 macrophages in the spleen, mesenteric lymph nodes, and colonic lamina propria. The levels of Th17- and Treg-associated cytokines were measured by quantitative polymerase chain reaction. The direct effect of H. pylori extract on the polarization status of macrophages was determined in vitro.
Results: Gastric H. pylori colonization significantly ameliorated the severity of chronic DSS-induced colitis. H. pylori colonization decreased Th17 cells and mRNA levels of IL-17A, IL-17F, and IL-21 in the colon. Simultaneously, H. pylori colonization increased Treg cells and IL-10 expression. As to cytokines driving Th17 and Treg differentiation, H. pylori colonization increased TGFβ and decreased IL-6 and IL-23. Moreover, H. pylori colonization significantly increased M2 macrophages in the colon. In vitro, H. pylori extract promotion of M2 macrophage polarization was dependent on the presence of CagA.
Conclusions: H. pylori colonization protects against chronic DSS-induced colitis via balancing Th17/Treg responses and shifting macrophages toward anti-inflammatory M2 phenotype. Our results strengthen the rationale for gastric H. pylori colonization affecting the immune homeostasis of the colon.
Full text links
Related Resources
Trending Papers
Autoimmune Hemolytic Anemias: Classifications, Pathophysiology, Diagnoses and Management.International Journal of Molecular Sciences 2024 April 13
Executive Summary: State-of-the-Art Review: Unintended Consequences: Risk of Opportunistic Infections Associated with Long-term Glucocorticoid Therapies in Adults.Clinical Infectious Diseases 2024 April 11
Clinical practice guidelines on the management of status epilepticus in adults: A systematic review.Epilepsia 2024 April 13
Finerenone: From the Mechanism of Action to Clinical Use in Kidney Disease.Pharmaceuticals 2024 March 27
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app