H.pylori Infection Alleviates Acute and Chronic Colitis with the Expansion of Regulatory B Cells in Mice
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ORIGINAL ARTICLE
H.pylori Infection Alleviates Acute and Chronic Colitis with the Expansion of Regulatory B Cells in Mice Xia Li,1 Jiang Tan,1 Feng Zhang,2 Qian Xue,1 Ning Wang,1 Xu Cong,3 and Jingtong Wang1,4
Epidemiological studies showed that there was an inverse relationship between Helicobacter pylori (H. pylori) infection and the incidence of inflammatory bowel diseases (IBD). Our previous research indicated that the regulatory immune responses induced by H. pylori infection were not limited to gastric mucosa, and the balance of intestinal mucosal immunity was influenced. In this study, mice were infected with H. pylori SS1, and then colitis was induced by 3% dextran sulphate sodium (DSS), to investigate the role of the regulatory B cells in the effects of H. pylori infection on acute and chronic colitis. In acute and chronic colitis groups, DAI and colonic histological scores reduced significantly and colon length shorted less, the proinflammatory cytokines mRNA expression downregulated in colonic mucosa, and the percentages of CD19+IL-10+Breg cells were higher in the H. pylori/ DSS co-treated groups compared with the DSS-treated groups. Our study suggests that H. pylori infection can alleviate the acute and chronic colitis induced by DSS, and CD19+IL10+Breg cells may play a critical role in the alleviation of acute and chronic colitis following H. pylori infection. Abstract—
KEY WORDS: Regulatory B cells; Helicobacter pylori; Inflammatory bowel diseases; Regulatory T cells.
INTRODUCTION Helicobacter pylori (H. pylori) is the predominant bacterium colonized in the stomach, and associated with several diseases including gastritis, peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphomas [1]. H. pylori infection cannot be cleared effectively even though it can elicit a series of immune
1
Department of Geratology, Peking University People’s Hospital, Beijing, 100044, China 2 Department of Gastroenterology, Peking University People’s Hospital, No. 11, Xizhimen South Street, Xicheng District, Beijing, 100044, China 3 Peking University Hepatology Institute, Peking University People’s Hospital, Beijing, 100044, China 4 To whom correspondence should be addressed at Department of Geratology, Peking University People’s Hospital, Beijing, 100044, China. E-mail: [email protected]
responses. The immunological escape is considered to be mediated by the immunosuppressive regulatory cells. Foxp3 expression can be induced by H. pylori infection, and there is no or less Foxp3 mRNA expression in the stomach without H. pylori infection [2, 3]. Gastritis caused by H. pylori is relieved by increased CD4 + CD25 + Foxp3+ marked regulatory T cells (Treg), which inhibit the Th1 and Th17 cells through the secretion of antiinflammatory cytokines (IL-10,TGF-β) and the manner of cell to cell contact [4, 5]. Our previous study showed that, besides the CD4+CD25+Foxp3+Treg cells, CD19 + IL-10+ marked regulatory B cells (Breg) also expanded significantly after H. pylori infection. The regulatory immune
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