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Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis
The gut microbiota were shown to play critical roles in the development of atherosclerosis, but the detailed mechanism is limited. The purpose of this study is to clarify the influence of gut microbiota on atherogenesis via lipid metabolism and systemic inflammation. Germ-free or conventionally rais...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Biochemistry and Molecular Biology
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5335582/ https://www.ncbi.nlm.nih.gov/pubmed/28130274 http://dx.doi.org/10.1194/jlr.M072165 |
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author | Kasahara, Kazuyuki Tanoue, Takeshi Yamashita, Tomoya Yodoi, Keiko Matsumoto, Takuya Emoto, Takuo Mizoguchi, Taiji Hayashi, Tomohiro Kitano, Naoki Sasaki, Naoto Atarashi, Koji Honda, Kenya Hirata, Ken-ichi |
author_facet | Kasahara, Kazuyuki Tanoue, Takeshi Yamashita, Tomoya Yodoi, Keiko Matsumoto, Takuya Emoto, Takuo Mizoguchi, Taiji Hayashi, Tomohiro Kitano, Naoki Sasaki, Naoto Atarashi, Koji Honda, Kenya Hirata, Ken-ichi |
author_sort | Kasahara, Kazuyuki |
collection | PubMed |
description | The gut microbiota were shown to play critical roles in the development of atherosclerosis, but the detailed mechanism is limited. The purpose of this study is to clarify the influence of gut microbiota on atherogenesis via lipid metabolism and systemic inflammation. Germ-free or conventionally raised (Conv) ApoE-deficient (ApoE(−/−)) mice were fed chow diet and euthanized at 20 weeks of age. We found that the lack of gut microbiota in ApoE(−/−) mice caused a significant increase in the plasma and hepatic cholesterol levels compared with Conv ApoE(−/−) mice. The absence of gut microbiota changed the bile acid composition in the ileum, which was associated with activation of the enterohepatic fibroblast growth factor 15, fibroblast growth factor receptor 4 axis, and reduction of cholesterol 7α-hydroxylase and hepatic bile acid synthesis, resulting in the accumulation of liver cholesterol content. However, we found that the lack of microbiota caused a significant reduction in atherosclerotic lesion formation compared with Conv ApoE(−/−) mice, which might be associated with the attenuation of lipopolysaccharide-mediated inflammatory responses. Our findings indicated that the gut microbiota affected both hypercholesterolemia and atherogenesis in mice. |
format | Online Article Text |
id | pubmed-5335582 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The American Society for Biochemistry and Molecular Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-53355822017-11-03 Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis Kasahara, Kazuyuki Tanoue, Takeshi Yamashita, Tomoya Yodoi, Keiko Matsumoto, Takuya Emoto, Takuo Mizoguchi, Taiji Hayashi, Tomohiro Kitano, Naoki Sasaki, Naoto Atarashi, Koji Honda, Kenya Hirata, Ken-ichi J Lipid Res Research Articles The gut microbiota were shown to play critical roles in the development of atherosclerosis, but the detailed mechanism is limited. The purpose of this study is to clarify the influence of gut microbiota on atherogenesis via lipid metabolism and systemic inflammation. Germ-free or conventionally raised (Conv) ApoE-deficient (ApoE(−/−)) mice were fed chow diet and euthanized at 20 weeks of age. We found that the lack of gut microbiota in ApoE(−/−) mice caused a significant increase in the plasma and hepatic cholesterol levels compared with Conv ApoE(−/−) mice. The absence of gut microbiota changed the bile acid composition in the ileum, which was associated with activation of the enterohepatic fibroblast growth factor 15, fibroblast growth factor receptor 4 axis, and reduction of cholesterol 7α-hydroxylase and hepatic bile acid synthesis, resulting in the accumulation of liver cholesterol content. However, we found that the lack of microbiota caused a significant reduction in atherosclerotic lesion formation compared with Conv ApoE(−/−) mice, which might be associated with the attenuation of lipopolysaccharide-mediated inflammatory responses. Our findings indicated that the gut microbiota affected both hypercholesterolemia and atherogenesis in mice. The American Society for Biochemistry and Molecular Biology 2017-03 2017-02-27 /pmc/articles/PMC5335582/ /pubmed/28130274 http://dx.doi.org/10.1194/jlr.M072165 Text en Copyright © 2017 by the American Society for Biochemistry and Molecular Biology, Inc. http://creativecommons.org/licenses/by/4.0/ Author’s Choice—Final version free via Creative Commons CC-BY license. |
spellingShingle | Research Articles Kasahara, Kazuyuki Tanoue, Takeshi Yamashita, Tomoya Yodoi, Keiko Matsumoto, Takuya Emoto, Takuo Mizoguchi, Taiji Hayashi, Tomohiro Kitano, Naoki Sasaki, Naoto Atarashi, Koji Honda, Kenya Hirata, Ken-ichi Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis |
title | Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis |
title_full | Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis |
title_fullStr | Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis |
title_full_unstemmed | Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis |
title_short | Commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis |
title_sort | commensal bacteria at the crossroad between cholesterol homeostasis and chronic inflammation in atherosclerosis |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5335582/ https://www.ncbi.nlm.nih.gov/pubmed/28130274 http://dx.doi.org/10.1194/jlr.M072165 |
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