title: IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses.
abstract: Interleukin- (IL-) 33, a member of the IL-1 cytokine family, is an important modulator of the immune system associated with several immune-mediated diseases. IL-33 was expressed in high level on epithelial cells of intestinal tract. It suggested that IL-33 plays a potential role in inflammatory bowel diseases (IBD). We investigated the role of interleukin- (IL-) 33 in dextran sulphate sodium- (DSS-) induced acute colitis in mice using recombinant mouse IL-33 protein (rIL-33). We found that DSS-induced acute colitis was aggravated by rIL-33 treatment. rIL-33-treated DSS mice showed markedly reduced levels of interferon- (IFN-)γ and IL-17A in their colon lamina propria lymphocytes (LPL), but the levels of Th2 cytokines, such as IL-5 and IL-13, in these cells were significantly increased, compared to DSS mice treated with PBS. Our results suggested that IL-33 stimulated CD4(+)T cells and caused the cell to adopt a Th2-type response but at the same time suppressed Th17 and Th1 cell responses. Therefore, IL-33 may be involved in pathogenesis of DSS-induced acute colitis by promoting Th2 cell response in intestinal mucosa of mice. Modulation of IL-33/ST2 signaling by monoclonal antibody (mAb) could be a novel biological therapy in DSS-induced acute colitis.
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China ; School of Life Science, Liaoning University, Shenyang 110036, China.
authors.forename: Junfeng
authors.initials: J
authors.lastname: Zhu
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Fangli
authors.initials: F
authors.lastname: Yang
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Lixuan
authors.initials: L
authors.lastname: Sang
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Jingbo
authors.initials: J
authors.lastname: Zhai
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Yue
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Shengjun
authors.initials: S
authors.lastname: Li
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Changlong
authors.initials: C
authors.lastname: Lu
authors.affiliation: Department of Immunology, China Medical University, Shenyang 110122, China.
authors.forename: Xun
authors.initials: X
authors.lastname: Sun
mesh_terms: D000208:Acute Disease; D000818:Animals; D003092:Colitis / Q000139:chemically induced* / Q000276:immunology; D016207:Cytokines / Q000096:biosynthesis; D016264:Dextran Sulfate / Q000633:toxicity; D000067596:Interleukin-33 / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011994:Recombinant Proteins / Q000494:pharmacology; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology; D014157:Transcription Factors / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D000067596:Interleukin-33; D011994:Recombinant Proteins; D014157:Transcription Factors; D016264:Dextran Sulfate