IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses
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 bowe...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/913041 |
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| author | Junfeng Zhu Fangli Yang Lixuan Sang Jingbo Zhai Xiaoqing Zhang Dan Yue Shengjun Li Yan Li Changlong Lu Xun Sun |
| author_facet | Junfeng Zhu Fangli Yang Lixuan Sang Jingbo Zhai Xiaoqing Zhang Dan Yue Shengjun Li Yan Li Changlong Lu Xun Sun |
| author_sort | Junfeng Zhu |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-ae821620ea244b85bfd721da485ea1d8 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-ae821620ea244b85bfd721da485ea1d82025-02-03T01:23:47ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/913041913041IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell ResponsesJunfeng Zhu0Fangli Yang1Lixuan Sang2Jingbo Zhai3Xiaoqing Zhang4Dan Yue5Shengjun Li6Yan Li7Changlong Lu8Xun Sun9Department of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaDepartment of Immunology, China Medical University, Shenyang 110122, ChinaInterleukin- (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.http://dx.doi.org/10.1155/2015/913041 |
| spellingShingle | Junfeng Zhu Fangli Yang Lixuan Sang Jingbo Zhai Xiaoqing Zhang Dan Yue Shengjun Li Yan Li Changlong Lu Xun Sun IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses Mediators of Inflammation |
| title | IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses |
| title_full | IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses |
| title_fullStr | IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses |
| title_full_unstemmed | IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses |
| title_short | IL-33 Aggravates DSS-Induced Acute Colitis in Mouse Colon Lamina Propria by Enhancing Th2 Cell Responses |
| title_sort | il 33 aggravates dss induced acute colitis in mouse colon lamina propria by enhancing th2 cell responses |
| url | http://dx.doi.org/10.1155/2015/913041 |
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