Research Papers:

H. pylori attenuates TNBS-induced colitis via increasing mucosal Th2 cells in mice

Yi-Zhong Wu, Gao Tan, Fang Wu and Fa-Chao Zhi _

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Oncotarget. 2017; 8:73810-73816. https://doi.org/10.18632/oncotarget.17962

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Yi-Zhong Wu1,2,*, Gao Tan1,*, Fang Wu3 and Fa-Chao Zhi1

1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China

2Department of Gastroenterology, Hunan Provincial People’s Hospital, Changsha, China

3Department of Gastroenterology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

*These authors contributed equally to this work

Correspondence to:

Fa-Chao Zhi, email: [email protected]

Gao Tan, email: [email protected]

Keywords: H. pylori, Crohn’s disease, mucosal immunology, Th cells

Received: September 26, 2016     Accepted: April 19, 2017     Published: May 18, 2017


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.

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