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Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function

The intestinal microbiota is critical for maintaining homeostasis. Dysbiosis, an imbalance in the microbial community, contributes to the susceptibility of several diseases. Many factors are known to influence gut microbial composition, including diet. We have previously shown that fecal immunoglobu...

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Autores principales: Brawner, Kyle M., Yeramilli, Venkata A., Duck, Lennard W., Van Der Pol, William, Smythies, Lesley E., Morrow, Casey D., Elson, Charles O., Martin, Colin A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6789125/
https://www.ncbi.nlm.nih.gov/pubmed/31604984
http://dx.doi.org/10.1038/s41598-019-51194-w
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author Brawner, Kyle M.
Yeramilli, Venkata A.
Duck, Lennard W.
Van Der Pol, William
Smythies, Lesley E.
Morrow, Casey D.
Elson, Charles O.
Martin, Colin A.
author_facet Brawner, Kyle M.
Yeramilli, Venkata A.
Duck, Lennard W.
Van Der Pol, William
Smythies, Lesley E.
Morrow, Casey D.
Elson, Charles O.
Martin, Colin A.
author_sort Brawner, Kyle M.
collection PubMed
description The intestinal microbiota is critical for maintaining homeostasis. Dysbiosis, an imbalance in the microbial community, contributes to the susceptibility of several diseases. Many factors are known to influence gut microbial composition, including diet. We have previously shown that fecal immunoglobulin (Ig) A levels are decreased in mice fed a diet free of aryl hydrocarbon receptor (AhR) ligands. Here, we hypothesize this IgA decrease is secondary to diet-induced dysbiosis. We assigned mice to a conventional diet, an AhR ligand-free diet, or an AhR ligand-free diet supplemented with the dietary AhR ligand indole-3-carbinol (I3C). We observed a global alteration of fecal microbiota upon dietary AhR ligand deprivation. Compared to mice on the conventional diet, family Erysipelotrichaceae was enriched in the feces of mice on the AhR ligand-free diet but returned to normal levels upon dietary supplementation with I3C. Faecalibaculum rodentium, an Erysipelotrichaceae species, depleted its growth media of AhR ligands. Cultured fecal bacteria from mice on the AhR ligand-free diet, but not the other two diets, were able to alter IgA levels in vitro, as was F. rodentium alone. Our data point to the critical role of AhR dietary ligands in shaping the composition and proper functioning of gut microbiota.
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spelling pubmed-67891252019-10-17 Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function Brawner, Kyle M. Yeramilli, Venkata A. Duck, Lennard W. Van Der Pol, William Smythies, Lesley E. Morrow, Casey D. Elson, Charles O. Martin, Colin A. Sci Rep Article The intestinal microbiota is critical for maintaining homeostasis. Dysbiosis, an imbalance in the microbial community, contributes to the susceptibility of several diseases. Many factors are known to influence gut microbial composition, including diet. We have previously shown that fecal immunoglobulin (Ig) A levels are decreased in mice fed a diet free of aryl hydrocarbon receptor (AhR) ligands. Here, we hypothesize this IgA decrease is secondary to diet-induced dysbiosis. We assigned mice to a conventional diet, an AhR ligand-free diet, or an AhR ligand-free diet supplemented with the dietary AhR ligand indole-3-carbinol (I3C). We observed a global alteration of fecal microbiota upon dietary AhR ligand deprivation. Compared to mice on the conventional diet, family Erysipelotrichaceae was enriched in the feces of mice on the AhR ligand-free diet but returned to normal levels upon dietary supplementation with I3C. Faecalibaculum rodentium, an Erysipelotrichaceae species, depleted its growth media of AhR ligands. Cultured fecal bacteria from mice on the AhR ligand-free diet, but not the other two diets, were able to alter IgA levels in vitro, as was F. rodentium alone. Our data point to the critical role of AhR dietary ligands in shaping the composition and proper functioning of gut microbiota. Nature Publishing Group UK 2019-10-11 /pmc/articles/PMC6789125/ /pubmed/31604984 http://dx.doi.org/10.1038/s41598-019-51194-w Text en © The Author(s) 2019 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
Brawner, Kyle M.
Yeramilli, Venkata A.
Duck, Lennard W.
Van Der Pol, William
Smythies, Lesley E.
Morrow, Casey D.
Elson, Charles O.
Martin, Colin A.
Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function
title Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function
title_full Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function
title_fullStr Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function
title_full_unstemmed Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function
title_short Depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function
title_sort depletion of dietary aryl hydrocarbon receptor ligands alters microbiota composition and function
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6789125/
https://www.ncbi.nlm.nih.gov/pubmed/31604984
http://dx.doi.org/10.1038/s41598-019-51194-w
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