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Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids
The life span of intestinal epithelial cells (IECs) is short (3–5 days), and its regulation is thought to be important for homeostasis of the intestinal epithelium. We have now investigated the role of commensal bacteria in regulation of IEC turnover in the small intestine. The proliferative activit...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4883796/ https://www.ncbi.nlm.nih.gov/pubmed/27232601 http://dx.doi.org/10.1371/journal.pone.0156334 |
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author | Park, Jung-ha Kotani, Takenori Konno, Tasuku Setiawan, Jajar Kitamura, Yasuaki Imada, Shinya Usui, Yutaro Hatano, Naoya Shinohara, Masakazu Saito, Yasuyuki Murata, Yoji Matozaki, Takashi |
author_facet | Park, Jung-ha Kotani, Takenori Konno, Tasuku Setiawan, Jajar Kitamura, Yasuaki Imada, Shinya Usui, Yutaro Hatano, Naoya Shinohara, Masakazu Saito, Yasuyuki Murata, Yoji Matozaki, Takashi |
author_sort | Park, Jung-ha |
collection | PubMed |
description | The life span of intestinal epithelial cells (IECs) is short (3–5 days), and its regulation is thought to be important for homeostasis of the intestinal epithelium. We have now investigated the role of commensal bacteria in regulation of IEC turnover in the small intestine. The proliferative activity of IECs in intestinal crypts as well as the migration of these cells along the crypt-villus axis were markedly attenuated both in germ-free mice and in specific pathogen–free (SPF) mice treated with a mixture of antibiotics, with antibiotics selective for Gram-positive bacteria being most effective in this regard. Oral administration of chloroform-treated feces of SPF mice to germ-free mice resulted in a marked increase in IEC turnover, suggesting that spore-forming Gram-positive bacteria contribute to this effect. Oral administration of short-chain fatty acids (SCFAs) as bacterial fermentation products also restored the turnover of IECs in antibiotic-treated SPF mice as well as promoted the development of intestinal organoids in vitro. Antibiotic treatment reduced the phosphorylation levels of ERK, ribosomal protein S6, and STAT3 in IECs of SPF mice. Our results thus suggest that Gram-positive commensal bacteria are a major determinant of IEC turnover, and that their stimulatory effect is mediated by SCFAs. |
format | Online Article Text |
id | pubmed-4883796 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-48837962016-06-10 Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids Park, Jung-ha Kotani, Takenori Konno, Tasuku Setiawan, Jajar Kitamura, Yasuaki Imada, Shinya Usui, Yutaro Hatano, Naoya Shinohara, Masakazu Saito, Yasuyuki Murata, Yoji Matozaki, Takashi PLoS One Research Article The life span of intestinal epithelial cells (IECs) is short (3–5 days), and its regulation is thought to be important for homeostasis of the intestinal epithelium. We have now investigated the role of commensal bacteria in regulation of IEC turnover in the small intestine. The proliferative activity of IECs in intestinal crypts as well as the migration of these cells along the crypt-villus axis were markedly attenuated both in germ-free mice and in specific pathogen–free (SPF) mice treated with a mixture of antibiotics, with antibiotics selective for Gram-positive bacteria being most effective in this regard. Oral administration of chloroform-treated feces of SPF mice to germ-free mice resulted in a marked increase in IEC turnover, suggesting that spore-forming Gram-positive bacteria contribute to this effect. Oral administration of short-chain fatty acids (SCFAs) as bacterial fermentation products also restored the turnover of IECs in antibiotic-treated SPF mice as well as promoted the development of intestinal organoids in vitro. Antibiotic treatment reduced the phosphorylation levels of ERK, ribosomal protein S6, and STAT3 in IECs of SPF mice. Our results thus suggest that Gram-positive commensal bacteria are a major determinant of IEC turnover, and that their stimulatory effect is mediated by SCFAs. Public Library of Science 2016-05-27 /pmc/articles/PMC4883796/ /pubmed/27232601 http://dx.doi.org/10.1371/journal.pone.0156334 Text en © 2016 Park et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Park, Jung-ha Kotani, Takenori Konno, Tasuku Setiawan, Jajar Kitamura, Yasuaki Imada, Shinya Usui, Yutaro Hatano, Naoya Shinohara, Masakazu Saito, Yasuyuki Murata, Yoji Matozaki, Takashi Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids |
title | Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids |
title_full | Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids |
title_fullStr | Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids |
title_full_unstemmed | Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids |
title_short | Promotion of Intestinal Epithelial Cell Turnover by Commensal Bacteria: Role of Short-Chain Fatty Acids |
title_sort | promotion of intestinal epithelial cell turnover by commensal bacteria: role of short-chain fatty acids |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4883796/ https://www.ncbi.nlm.nih.gov/pubmed/27232601 http://dx.doi.org/10.1371/journal.pone.0156334 |
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