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Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons

Endometriosis is defined as the growth of endometrial tissue in ectopic locations, and is associated with altered immune and microbial phenotypes. It is unclear if these changes are the result of the disease or may be causative. We induced endometriosis in non-human primates (Papio Anubis) to test o...

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Autores principales: Le, Nhung, Cregger, Melissa, Fazleabas, Asgerally, Braundmeier-Fleming, Andrea
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803974/
https://www.ncbi.nlm.nih.gov/pubmed/35102185
http://dx.doi.org/10.1038/s41598-022-05499-y
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author Le, Nhung
Cregger, Melissa
Fazleabas, Asgerally
Braundmeier-Fleming, Andrea
author_facet Le, Nhung
Cregger, Melissa
Fazleabas, Asgerally
Braundmeier-Fleming, Andrea
author_sort Le, Nhung
collection PubMed
description Endometriosis is defined as the growth of endometrial tissue in ectopic locations, and is associated with altered immune and microbial phenotypes. It is unclear if these changes are the result of the disease or may be causative. We induced endometriosis in non-human primates (Papio Anubis) to test our hypothesis that the growth of endometriotic lesions results in alterations in immune and microbial dynamics that may advance disease progression. Baboon samples were collected pre-inoculation (prior to disease induction), at 3, 6, 9, and 15 months after disease induction. Tolerant regulatory T-cells (Tregs) and inflammatory T-helper 17 (Th17) cells were identified in peripheral blood and within the eutopic/ectopic endometrial tissues. Microbiome communities were identified in fecal/urine samples. The induction of endometriosis decreased peripheral Tregs cells while Th17 cells increased at all post-induction collections, thus reducing the Tregs:Th17 cells ratio, indicating systemic inflammation. Microbiome diversity and abundance were altered at each sample site after disease induction. Thus, induction of endometriosis in baboons caused an immune shift toward an inflammatory profile and altered mucosal microbial profiles, which may drive inflammation through production of inflammatory mediators. Immune and microbial profiling may lead to innovative diagnostic tools and novel therapies for endometriosis treatment.
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spelling pubmed-88039742022-02-01 Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons Le, Nhung Cregger, Melissa Fazleabas, Asgerally Braundmeier-Fleming, Andrea Sci Rep Article Endometriosis is defined as the growth of endometrial tissue in ectopic locations, and is associated with altered immune and microbial phenotypes. It is unclear if these changes are the result of the disease or may be causative. We induced endometriosis in non-human primates (Papio Anubis) to test our hypothesis that the growth of endometriotic lesions results in alterations in immune and microbial dynamics that may advance disease progression. Baboon samples were collected pre-inoculation (prior to disease induction), at 3, 6, 9, and 15 months after disease induction. Tolerant regulatory T-cells (Tregs) and inflammatory T-helper 17 (Th17) cells were identified in peripheral blood and within the eutopic/ectopic endometrial tissues. Microbiome communities were identified in fecal/urine samples. The induction of endometriosis decreased peripheral Tregs cells while Th17 cells increased at all post-induction collections, thus reducing the Tregs:Th17 cells ratio, indicating systemic inflammation. Microbiome diversity and abundance were altered at each sample site after disease induction. Thus, induction of endometriosis in baboons caused an immune shift toward an inflammatory profile and altered mucosal microbial profiles, which may drive inflammation through production of inflammatory mediators. Immune and microbial profiling may lead to innovative diagnostic tools and novel therapies for endometriosis treatment. Nature Publishing Group UK 2022-01-31 /pmc/articles/PMC8803974/ /pubmed/35102185 http://dx.doi.org/10.1038/s41598-022-05499-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Le, Nhung
Cregger, Melissa
Fazleabas, Asgerally
Braundmeier-Fleming, Andrea
Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons
title Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons
title_full Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons
title_fullStr Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons
title_full_unstemmed Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons
title_short Effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons
title_sort effects of endometriosis on immunity and mucosal microbial community dynamics in female olive baboons
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803974/
https://www.ncbi.nlm.nih.gov/pubmed/35102185
http://dx.doi.org/10.1038/s41598-022-05499-y
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