Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease

Abstract Interleukin 33 (IL-33) that signals through the ST2 receptor has emerged as a critical modulator in several inflammatory disorders, including inflammatory bowel disease (IBD). However, the precise mechanisms by which IL-33 modulates IBD are controversial. The aim of this study was thus to c...

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Autores principales:	Dong Hyuk Seo, Xiumei Che, Min Seob Kwak, Soochan Kim, Jae Hyeon Kim, Hyun Woo Ma, Da Hye Kim, Tae Il Kim, Won Ho Kim, Seung Won Kim, Jae Hee Cheon
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7f1047a4c7574a95b9c6d876b38dec88
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spelling	oai:doaj.org-article:7f1047a4c7574a95b9c6d876b38dec882021-12-02T11:41:20ZInterleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease10.1038/s41598-017-00840-22045-2322https://doaj.org/article/7f1047a4c7574a95b9c6d876b38dec882017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00840-2https://doaj.org/toc/2045-2322Abstract Interleukin 33 (IL-33) that signals through the ST2 receptor has emerged as a critical modulator in several inflammatory disorders, including inflammatory bowel disease (IBD). However, the precise mechanisms by which IL-33 modulates IBD are controversial. The aim of this study was thus to clarify the role of IL-33 in IBD. The plasma levels of IL-33 were significantly decreased, but soluble ST2 levels were increased in patients with IBD compared to healthy individuals. Moreover, IL-33 restored goblet cell numbers and induced macrophage switching from the M1 to the M2 phenotype. These effects were sufficient to ameliorate colitis in dextran sodium sulfate, trinitrobenzene sulfonic acid, and peritoneal cavity cell transfer models. IL-33 facilitated goblet cell restoration via modulating macrophages toward the M2 phenotype. In addition, wound healing was significantly faster in IL-33-treated human monocyte-derived macrophages than in control cells, which could be attributed to increased polarisation into M2 macrophages. We found that patients with IBD show decreased serum levels of IL-33 compared with healthy individuals and that IL-33 can attenuate colitis and aid tissue repair in mice. The mechanism by which IL-33 exerts these effects appears to involve the stimulation of differentiation of goblet cells and M2 macrophages.Dong Hyuk SeoXiumei CheMin Seob KwakSoochan KimJae Hyeon KimHyun Woo MaDa Hye KimTae Il KimWon Ho KimSeung Won KimJae Hee CheonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Dong Hyuk Seo Xiumei Che Min Seob Kwak Soochan Kim Jae Hyeon Kim Hyun Woo Ma Da Hye Kim Tae Il Kim Won Ho Kim Seung Won Kim Jae Hee Cheon Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease
description	Abstract Interleukin 33 (IL-33) that signals through the ST2 receptor has emerged as a critical modulator in several inflammatory disorders, including inflammatory bowel disease (IBD). However, the precise mechanisms by which IL-33 modulates IBD are controversial. The aim of this study was thus to clarify the role of IL-33 in IBD. The plasma levels of IL-33 were significantly decreased, but soluble ST2 levels were increased in patients with IBD compared to healthy individuals. Moreover, IL-33 restored goblet cell numbers and induced macrophage switching from the M1 to the M2 phenotype. These effects were sufficient to ameliorate colitis in dextran sodium sulfate, trinitrobenzene sulfonic acid, and peritoneal cavity cell transfer models. IL-33 facilitated goblet cell restoration via modulating macrophages toward the M2 phenotype. In addition, wound healing was significantly faster in IL-33-treated human monocyte-derived macrophages than in control cells, which could be attributed to increased polarisation into M2 macrophages. We found that patients with IBD show decreased serum levels of IL-33 compared with healthy individuals and that IL-33 can attenuate colitis and aid tissue repair in mice. The mechanism by which IL-33 exerts these effects appears to involve the stimulation of differentiation of goblet cells and M2 macrophages.
format	article
author	Dong Hyuk Seo Xiumei Che Min Seob Kwak Soochan Kim Jae Hyeon Kim Hyun Woo Ma Da Hye Kim Tae Il Kim Won Ho Kim Seung Won Kim Jae Hee Cheon
author_facet	Dong Hyuk Seo Xiumei Che Min Seob Kwak Soochan Kim Jae Hyeon Kim Hyun Woo Ma Da Hye Kim Tae Il Kim Won Ho Kim Seung Won Kim Jae Hee Cheon
author_sort	Dong Hyuk Seo
title	Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease
title_short	Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease
title_full	Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease
title_fullStr	Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease
title_full_unstemmed	Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease
title_sort	interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/7f1047a4c7574a95b9c6d876b38dec88
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Interleukin-33 regulates intestinal inflammation by modulating macrophages in inflammatory bowel disease

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