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The bidirectional relationship between endometriosis and microbiome

Endometriosis has been described by many different theories of pathogenesis over the years. It is now also appreciated to be a state of chronic inflammation, and the role of immune dysfunction in its development has been proven. There is increasing evidence to support the role of the microbiome in t...

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Autores principales: Uzuner, Cansu, Mak, Jason, El-Assaad, Fatima, Condous, George
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10028178/
https://www.ncbi.nlm.nih.gov/pubmed/36960395
http://dx.doi.org/10.3389/fendo.2023.1110824
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author Uzuner, Cansu
Mak, Jason
El-Assaad, Fatima
Condous, George
author_facet Uzuner, Cansu
Mak, Jason
El-Assaad, Fatima
Condous, George
author_sort Uzuner, Cansu
collection PubMed
description Endometriosis has been described by many different theories of pathogenesis over the years. It is now also appreciated to be a state of chronic inflammation, and the role of immune dysfunction in its development has been proven. There is increasing evidence to support the role of the microbiome in the formation and progression of endometriosis via inflammatory pathways. The dysbiosis seen in endometriosis is thought to be both causative and a consequence of the pathogenesis. Gut, peritoneal fluid and female reproductive tract microbiota has been studied to understand if there are any microbiome signatures specific to endometriosis. New research on how to manipulate the microbiome for better detection and treatment of endometriosis is emerging.
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spelling pubmed-100281782023-03-22 The bidirectional relationship between endometriosis and microbiome Uzuner, Cansu Mak, Jason El-Assaad, Fatima Condous, George Front Endocrinol (Lausanne) Endocrinology Endometriosis has been described by many different theories of pathogenesis over the years. It is now also appreciated to be a state of chronic inflammation, and the role of immune dysfunction in its development has been proven. There is increasing evidence to support the role of the microbiome in the formation and progression of endometriosis via inflammatory pathways. The dysbiosis seen in endometriosis is thought to be both causative and a consequence of the pathogenesis. Gut, peritoneal fluid and female reproductive tract microbiota has been studied to understand if there are any microbiome signatures specific to endometriosis. New research on how to manipulate the microbiome for better detection and treatment of endometriosis is emerging. Frontiers Media S.A. 2023-03-07 /pmc/articles/PMC10028178/ /pubmed/36960395 http://dx.doi.org/10.3389/fendo.2023.1110824 Text en Copyright © 2023 Uzuner, Mak, El-Assaad and Condous https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Uzuner, Cansu
Mak, Jason
El-Assaad, Fatima
Condous, George
The bidirectional relationship between endometriosis and microbiome
title The bidirectional relationship between endometriosis and microbiome
title_full The bidirectional relationship between endometriosis and microbiome
title_fullStr The bidirectional relationship between endometriosis and microbiome
title_full_unstemmed The bidirectional relationship between endometriosis and microbiome
title_short The bidirectional relationship between endometriosis and microbiome
title_sort bidirectional relationship between endometriosis and microbiome
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10028178/
https://www.ncbi.nlm.nih.gov/pubmed/36960395
http://dx.doi.org/10.3389/fendo.2023.1110824
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