Bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.

Although some bacterial strains show potential to prevent colitis, their mechanisms are not fully understood. Here, we investigated the anti-colitic mechanisms of Bifidobacterium longum subsp. infantis JCM 1222(T), focusing on the relationship between interleukin (IL)-17A secreting CD4(+) T cells an...

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Autores principales: Eiji Miyauchi, Tasuku Ogita, Junki Miyamoto, Seiji Kawamoto, Hidetoshi Morita, Hiroshi Ohno, Takuya Suzuki, Soichi Tanabe
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Publicado: Public Library of Science (PLoS) 2013
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spelling oai:doaj.org-article:8e34d9bf0cff4a7ca033f1763a0ff4bc2021-11-18T08:47:38ZBifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.1932-620310.1371/journal.pone.0079735https://doaj.org/article/8e34d9bf0cff4a7ca033f1763a0ff4bc2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24255712/?tool=EBIhttps://doaj.org/toc/1932-6203Although some bacterial strains show potential to prevent colitis, their mechanisms are not fully understood. Here, we investigated the anti-colitic mechanisms of Bifidobacterium longum subsp. infantis JCM 1222(T), focusing on the relationship between interleukin (IL)-17A secreting CD4(+) T cells and intestinal epithelial costimulatory molecules in mice. Oral administration of JCM 1222(T) to mice alleviated dextran sulfate sodium (DSS)-induced acute colitis. The expression of type 1 helper T (Th1)- and IL-17 producing helper T (Th17)-specific cytokines and transcriptional factors was suppressed by JCM 1222(T) treatment. Intestinal epithelial cells (IECs) from colitic mice induced IL-17A production from CD4(+) T cells in a cell-cell contact-dependent manner, and this was suppressed by oral treatment with JCM 1222(T). Using blocking antibodies for costimulatory molecules, we revealed that epithelial costimulatory molecules including CD80 and CD40, which were highly expressed in IECs from colitic mice, were involved in IEC-induced IL-17A response. Treatment of mice and intestinal epithelial cell line Colon-26 cells with JCM 1222(T) decreased the expression of CD80 and CD40. Collectively, these data indicate that JCM 1222(T) negatively regulate epithelial costimulatory molecules, and this effect might be attributed, at least in part, to suppression of IL-17A in DSS-induced colitis.Eiji MiyauchiTasuku OgitaJunki MiyamotoSeiji KawamotoHidetoshi MoritaHiroshi OhnoTakuya SuzukiSoichi TanabePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 11, p e79735 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Eiji Miyauchi
Tasuku Ogita
Junki Miyamoto
Seiji Kawamoto
Hidetoshi Morita
Hiroshi Ohno
Takuya Suzuki
Soichi Tanabe
Bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.
description Although some bacterial strains show potential to prevent colitis, their mechanisms are not fully understood. Here, we investigated the anti-colitic mechanisms of Bifidobacterium longum subsp. infantis JCM 1222(T), focusing on the relationship between interleukin (IL)-17A secreting CD4(+) T cells and intestinal epithelial costimulatory molecules in mice. Oral administration of JCM 1222(T) to mice alleviated dextran sulfate sodium (DSS)-induced acute colitis. The expression of type 1 helper T (Th1)- and IL-17 producing helper T (Th17)-specific cytokines and transcriptional factors was suppressed by JCM 1222(T) treatment. Intestinal epithelial cells (IECs) from colitic mice induced IL-17A production from CD4(+) T cells in a cell-cell contact-dependent manner, and this was suppressed by oral treatment with JCM 1222(T). Using blocking antibodies for costimulatory molecules, we revealed that epithelial costimulatory molecules including CD80 and CD40, which were highly expressed in IECs from colitic mice, were involved in IEC-induced IL-17A response. Treatment of mice and intestinal epithelial cell line Colon-26 cells with JCM 1222(T) decreased the expression of CD80 and CD40. Collectively, these data indicate that JCM 1222(T) negatively regulate epithelial costimulatory molecules, and this effect might be attributed, at least in part, to suppression of IL-17A in DSS-induced colitis.
format article
author Eiji Miyauchi
Tasuku Ogita
Junki Miyamoto
Seiji Kawamoto
Hidetoshi Morita
Hiroshi Ohno
Takuya Suzuki
Soichi Tanabe
author_facet Eiji Miyauchi
Tasuku Ogita
Junki Miyamoto
Seiji Kawamoto
Hidetoshi Morita
Hiroshi Ohno
Takuya Suzuki
Soichi Tanabe
author_sort Eiji Miyauchi
title Bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.
title_short Bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.
title_full Bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.
title_fullStr Bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.
title_full_unstemmed Bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing IL-17A response: involvement of intestinal epithelial costimulatory molecules.
title_sort bifidobacterium longum alleviates dextran sulfate sodium-induced colitis by suppressing il-17a response: involvement of intestinal epithelial costimulatory molecules.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/8e34d9bf0cff4a7ca033f1763a0ff4bc
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