IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis

Abstract IL-33 is upregulated in ulcerative colitis and has a protective role in chemically-induced acute murine colitis. We aimed to determine whether IL-33 influences Il10 −/− chronic colitis and its cellular source in health and during colitis. Il10 −/− Il33 −/− and Il10 −/− Il33 +/+ littermates...

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Autores principales:	Amanda Waddell, Jefferson E. Vallance, Sejal Fox, Michael J. Rosen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9ba6bf1031684756b61c33a2778032d4
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spelling	oai:doaj.org-article:9ba6bf1031684756b61c33a2778032d42021-12-02T14:42:52ZIL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis10.1038/s41598-021-89119-12045-2322https://doaj.org/article/9ba6bf1031684756b61c33a2778032d42021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-89119-1https://doaj.org/toc/2045-2322Abstract IL-33 is upregulated in ulcerative colitis and has a protective role in chemically-induced acute murine colitis. We aimed to determine whether IL-33 influences Il10 −/− chronic colitis and its cellular source in health and during colitis. Il10 −/− Il33 −/− and Il10 −/− Il33 +/+ littermates developed colitis of similar severity. Colon Il33 was induced in WT and Il10 −/− mice exposed to DSS, but not in unchallenged Il10 −/− mice with colitis. Il33-citrine reporter mice showed that Il33-citrine colocalized with α-smooth muscle actin+ myofibroblasts and vimentin+ fibroblasts in WT mice. Citrine+CD74+CD90hi inflammatory fibroblasts were increased with DSS treatment. IL-1β induced Il33 expression in colon myofibroblasts, but colon Il33 expression did not differ between DSS-treated WT and Il1r1 −/− mice. In conclusion, deficiency of IL-33 does not alter the severity of chronic colitis in Il10 −/− mice. Induction of Il33 upon DSS exposure in WT and Il10 −/− mice, but not in unchallenged Il10 −/− mice, suggests epithelial injury induces colon IL-33. Fibroblasts are the primary colonic source of IL-33 and IL-33-expressing CD90hiCD74+ fibroblasts are increased during DSS-induced colitis. IL-1β induces Il33 in colon myofibroblasts in vitro, but signaling through the IL-1R1 is not necessary for induction of IL-33 in DSS-induced colitis.Amanda WaddellJefferson E. VallanceSejal FoxMichael J. RosenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Amanda Waddell Jefferson E. Vallance Sejal Fox Michael J. Rosen IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis
description	Abstract IL-33 is upregulated in ulcerative colitis and has a protective role in chemically-induced acute murine colitis. We aimed to determine whether IL-33 influences Il10 −/− chronic colitis and its cellular source in health and during colitis. Il10 −/− Il33 −/− and Il10 −/− Il33 +/+ littermates developed colitis of similar severity. Colon Il33 was induced in WT and Il10 −/− mice exposed to DSS, but not in unchallenged Il10 −/− mice with colitis. Il33-citrine reporter mice showed that Il33-citrine colocalized with α-smooth muscle actin+ myofibroblasts and vimentin+ fibroblasts in WT mice. Citrine+CD74+CD90hi inflammatory fibroblasts were increased with DSS treatment. IL-1β induced Il33 expression in colon myofibroblasts, but colon Il33 expression did not differ between DSS-treated WT and Il1r1 −/− mice. In conclusion, deficiency of IL-33 does not alter the severity of chronic colitis in Il10 −/− mice. Induction of Il33 upon DSS exposure in WT and Il10 −/− mice, but not in unchallenged Il10 −/− mice, suggests epithelial injury induces colon IL-33. Fibroblasts are the primary colonic source of IL-33 and IL-33-expressing CD90hiCD74+ fibroblasts are increased during DSS-induced colitis. IL-1β induces Il33 in colon myofibroblasts in vitro, but signaling through the IL-1R1 is not necessary for induction of IL-33 in DSS-induced colitis.
format	article
author	Amanda Waddell Jefferson E. Vallance Sejal Fox Michael J. Rosen
author_facet	Amanda Waddell Jefferson E. Vallance Sejal Fox Michael J. Rosen
author_sort	Amanda Waddell
title	IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis
title_short	IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis
title_full	IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis
title_fullStr	IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis
title_full_unstemmed	IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis
title_sort	il-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/9ba6bf1031684756b61c33a2778032d4
work_keys_str_mv	AT amandawaddell il33isproducedbycolonfibroblastsanddifferentiallyregulatedinacuteandchronicmurinecolitis AT jeffersonevallance il33isproducedbycolonfibroblastsanddifferentiallyregulatedinacuteandchronicmurinecolitis AT sejalfox il33isproducedbycolonfibroblastsanddifferentiallyregulatedinacuteandchronicmurinecolitis AT michaeljrosen il33isproducedbycolonfibroblastsanddifferentiallyregulatedinacuteandchronicmurinecolitis
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IL-33 is produced by colon fibroblasts and differentially regulated in acute and chronic murine colitis

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