Abstract
There is an epidemiological inverse relationship between Helicobacter pylori (H. pylori) infection and Crohn’s disease (CD). However, whether H. pylori plays a protective role against CD remains unclear. Since 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-induced colitis is thought to resemble CD, we investigated whether H. pylori can attenuate TNBS-induced colitis in mice. Here we show that H. pylori can attenuate the severity of TNBS-induced colitis. In addition, H. pylori not only down-regulates Th17 and Th1 cytokine expression, but can up-regulate Th2 cytokine expression and increase the Th2:Th17 ratio of CD4+ T in the colonic mucosa of TNBS-induced colitis. Our results indicate that H. pylori attenuates TNBS-induced colitis mainly through increasing Th2 cells in murine colonic mucosa. Our finding offers a novel view on the role of H. pylori in regulating gastrointestinal immunity, and may open a new avenue for development of therapeutic strategies in CD by making use of asymptomatic H. pylori colonization.
Highlights
Crohn’s disease (CD), one type of inflammatory bowel disease (IBD) [1], is a life-long, chronic and relapsing disease that may occur anywhere in the gastrointestinal tract [2, 3]
In order to determine whether H. pylori attenuates the severity of trinitrobenzene sulfonic acid (TNBS)-induced colitis, we treated mice with NCTC11639 after administration of TNBS enema and compared the disease activity scores, the colonic weight changes and the macroscopic and microscopic appearances of colons between mice treated with TNBS plus NCTC11639 and mice treated with TNBS only
This study is focused on exploring whether H. pylori plays a protective role against CD and the potential protective mechanism
Summary
Crohn’s disease (CD), one type of inflammatory bowel disease (IBD) [1], is a life-long, chronic and relapsing disease that may occur anywhere in the gastrointestinal tract [2, 3]. Helicobacter pylori (H. pylori), a highly adaptive gram-negative bacterium colonized the human gastric mucosa, has co-existed with humans for over 50,000 years [5, 6]. It is positively correlated with the pathogenesis of gastric ulcers, gastric cancers and mucosaassociated lymphoid tissue lymphoma, less than 15% and 1% of infected patients will develop gastric ulcer and cancer, respectively [7, 8]. Some reports have shown that there are rapid and clinical onset of CD after eradication of H. pylori infection [13, 14]. These researches found an inverse relationship between H. pylori infection and CD, whether H. pylori plays a protective role against CD and the potential protective mechanism remain unclear
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