title: IL-33 alleviates DSS-induced chronic colitis in C57BL/6 mice colon lamina propria by suppressing Th17 cell response as well as Th1 cell response.
abstract: Interleukin (IL)-33, a member of the IL-1 cytokine family, is associated with autoimmune diseases including inflammatory bowel diseases (IBD). A few studies on animal models have shown that IL-33 can suppress Th1 cell response and improve Th2 cell response in mesenteric lymph nodes (MLN) and sera. However, there is little data published about the effect of IL-33 on Th17 cell in and Th1/Th2 cell in colon lamina propria. The aim of this study was to investigate the effect of IL-33 on Th17 cell in colon lamina propria of mice with dextran sulfate sodium (DSS) induced chronic colitis. We studied the influence of IL-33 on colonic tissue injury and clinical symptoms of colitis. The T cell subsets were measured by flow cytometry and the production of cytokines secreted by lamina propria lymphocytes (LPL) was measured by Enzyme-Linked Immunosorbent Assay (ELISA) and quantitative real-time PCR. We have found that rIL-33 treatment led to a significant alleviation of DSS induced chronic colitis as evidenced by 1) alleviation of weight loss, DAI, macroscopic changes and histological score; 2) down-regulating the rates and absolute cell numbers of Th17 and Th1 cell in LPL; 3) inducing secretion of lower levels of IFN-γ and IL-17A. It is therefore concluded that IL-33 may play a therapeutic role in DSS-induced chronic colitis in mice by suppressing Th17 response and switching Th1 to Th2 response.
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China; Life Science School, Liaoning University, Shenyang, China.
authors.forename: Junfeng
authors.initials: J
authors.lastname: Zhu
authors.affiliation: The Fourth Affiliated Hospital of China Medical University, Shenyang, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China.
authors.forename: Fangli
authors.initials: F
authors.lastname: Yang
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China.
authors.forename: Lixuan
authors.initials: L
authors.lastname: Sang
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China.
authors.forename: Jingbo
authors.initials: J
authors.lastname: Zhai
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China.
authors.forename: Shengjun
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China.
authors.forename: Danan
authors.initials: D
authors.lastname: Wang
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China. Electronic address: cllu@mail.cmu.edu.cn.
authors.forename: Changlong
authors.initials: C
authors.lastname: Lu
authors.affiliation: Department of Immunology, China Medical University, Shenyang, China.
authors.forename: Xun
authors.initials: X
authors.lastname: Sun
mesh_terms: D000818:Animals; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology*; D003106:Colon / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000096:biosynthesis; D016264:Dextran Sulfate; D000067596:Interleukin-33 / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018417:Th1 Cells / Q000187:drug effects* / Q000276:immunology; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology; D015431:Weight Loss / Q000187:drug effects
chemical_list: D016207:Cytokines; D000067596:Interleukin-33; D016264:Dextran Sulfate
keywords: Colitis; Dextran sulfate sodium; IL-33, Th17/Th1 cell response