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Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress

Psychological stress can cause dysfunction of the gastrointestinal tract by regulating its interaction with central nervous system (brain-gut axis). Chronic social defeat stress (CSDS) is widely used to produce a rodent model of stress-induced human mood disorders and depression. We previously showe...

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Autores principales: Omata, Yasuhiro, Aoki, Reiji, Aoki-Yoshida, Ayako, Hiemori, Keiko, Toyoda, Atsushi, Tateno, Hiroaki, Suzuki, Chise, Takayama, Yoshiharu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6123462/
https://www.ncbi.nlm.nih.gov/pubmed/30181591
http://dx.doi.org/10.1038/s41598-018-31403-8
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author Omata, Yasuhiro
Aoki, Reiji
Aoki-Yoshida, Ayako
Hiemori, Keiko
Toyoda, Atsushi
Tateno, Hiroaki
Suzuki, Chise
Takayama, Yoshiharu
author_facet Omata, Yasuhiro
Aoki, Reiji
Aoki-Yoshida, Ayako
Hiemori, Keiko
Toyoda, Atsushi
Tateno, Hiroaki
Suzuki, Chise
Takayama, Yoshiharu
author_sort Omata, Yasuhiro
collection PubMed
description Psychological stress can cause dysfunction of the gastrointestinal tract by regulating its interaction with central nervous system (brain-gut axis). Chronic social defeat stress (CSDS) is widely used to produce a rodent model of stress-induced human mood disorders and depression. We previously showed that CSDS significantly affects the intestinal ecosystem including cecal and fecal microbiota, intestinal gene expression profiles and cecal metabolite profiles. Here, we investigated whether the glycosylation pattern in the intestinal epithelium was affected in C57BL/6 mice exposed to CSDS (hereinafter referred to as CSDS mice). A lectin microarray analysis revealed that CSDS significantly reduced the reactivity of fucose-specific lectins (rAOL, TJA-II, rAAL, rGC2, AOL, AAL, rPAIIL and rRSIIL) with distal intestinal mucosa, but not with mucosa from proximal intestine and colon. Flow cytometric analysis confirmed the reduced TJA-II reactivity with intestinal epithelial cells in CSDS mice. In addition, distal intestine expression levels of the genes encoding fucosyltransferase 1 and 2 (Fut1 and Fut2) were downregulated in CSDS mice. These findings suggest that CSDS alters the fucosylation pattern in the distal intestinal epithelium, which could be used as a sensitive marker for CSDS exposure.
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spelling pubmed-61234622018-09-10 Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress Omata, Yasuhiro Aoki, Reiji Aoki-Yoshida, Ayako Hiemori, Keiko Toyoda, Atsushi Tateno, Hiroaki Suzuki, Chise Takayama, Yoshiharu Sci Rep Article Psychological stress can cause dysfunction of the gastrointestinal tract by regulating its interaction with central nervous system (brain-gut axis). Chronic social defeat stress (CSDS) is widely used to produce a rodent model of stress-induced human mood disorders and depression. We previously showed that CSDS significantly affects the intestinal ecosystem including cecal and fecal microbiota, intestinal gene expression profiles and cecal metabolite profiles. Here, we investigated whether the glycosylation pattern in the intestinal epithelium was affected in C57BL/6 mice exposed to CSDS (hereinafter referred to as CSDS mice). A lectin microarray analysis revealed that CSDS significantly reduced the reactivity of fucose-specific lectins (rAOL, TJA-II, rAAL, rGC2, AOL, AAL, rPAIIL and rRSIIL) with distal intestinal mucosa, but not with mucosa from proximal intestine and colon. Flow cytometric analysis confirmed the reduced TJA-II reactivity with intestinal epithelial cells in CSDS mice. In addition, distal intestine expression levels of the genes encoding fucosyltransferase 1 and 2 (Fut1 and Fut2) were downregulated in CSDS mice. These findings suggest that CSDS alters the fucosylation pattern in the distal intestinal epithelium, which could be used as a sensitive marker for CSDS exposure. Nature Publishing Group UK 2018-09-04 /pmc/articles/PMC6123462/ /pubmed/30181591 http://dx.doi.org/10.1038/s41598-018-31403-8 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Omata, Yasuhiro
Aoki, Reiji
Aoki-Yoshida, Ayako
Hiemori, Keiko
Toyoda, Atsushi
Tateno, Hiroaki
Suzuki, Chise
Takayama, Yoshiharu
Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress
title Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress
title_full Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress
title_fullStr Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress
title_full_unstemmed Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress
title_short Reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress
title_sort reduced fucosylation in the distal intestinal epithelium of mice subjected to chronic social defeat stress
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6123462/
https://www.ncbi.nlm.nih.gov/pubmed/30181591
http://dx.doi.org/10.1038/s41598-018-31403-8
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