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

// Yi-Zhong Wu 1, 2, * , Gao Tan 1, * , Fang Wu 3 and Fa-Chao Zhi 1 1 Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China 2 Department of Gastroenterology, Hunan Provincial People’s Hospital, Changsha, China 3 Department 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: zhifc41532@163.com Gao Tan, email: tgao0316@163.com Keywords: H. pylori, Crohn’s disease, mucosal immunology, Th cells Received: September 26, 2016 Accepted: April 19, 2017 Published: May 18, 2017 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.