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Bile Acid Signaling in Inflammatory Bowel Disease

Inflammatory bowel disease is a chronic, idiopathic and complex condition, which most often manifests itself in the form of ulcerative colitis or Crohn’s disease. Both forms are associated with dysregulation of the mucosal immune system, compromised intestinal epithelial barrier, and dysbiosis of th...

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Autores principales: Bromke, Mariusz A., Krzystek-Korpacka, Małgorzata
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8396648/
https://www.ncbi.nlm.nih.gov/pubmed/34445800
http://dx.doi.org/10.3390/ijms22169096
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author Bromke, Mariusz A.
Krzystek-Korpacka, Małgorzata
author_facet Bromke, Mariusz A.
Krzystek-Korpacka, Małgorzata
author_sort Bromke, Mariusz A.
collection PubMed
description Inflammatory bowel disease is a chronic, idiopathic and complex condition, which most often manifests itself in the form of ulcerative colitis or Crohn’s disease. Both forms are associated with dysregulation of the mucosal immune system, compromised intestinal epithelial barrier, and dysbiosis of the gut microbiome. It has been observed for a long time that bile acids are involved in inflammatory disorders, and recent studies show their significant physiological role, reaching far beyond being emulsifiers helping in digestion of lipids. Bile acids are also signaling molecules, which act, among other things, on lipid metabolism and immune responses, through several nuclear and membrane receptors in hepatocytes, enterocytes and cells of the immune system. Gut microbiota homeostasis also seems to be affected, directly and indirectly, by bile acid metabolism and signaling. This review summarizes recent advances in the field of bile acid signaling, studies of inflamed gut microbiome, and the therapeutic potential of bile acids in the context of inflammatory bowel disease.
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spelling pubmed-83966482021-08-28 Bile Acid Signaling in Inflammatory Bowel Disease Bromke, Mariusz A. Krzystek-Korpacka, Małgorzata Int J Mol Sci Review Inflammatory bowel disease is a chronic, idiopathic and complex condition, which most often manifests itself in the form of ulcerative colitis or Crohn’s disease. Both forms are associated with dysregulation of the mucosal immune system, compromised intestinal epithelial barrier, and dysbiosis of the gut microbiome. It has been observed for a long time that bile acids are involved in inflammatory disorders, and recent studies show their significant physiological role, reaching far beyond being emulsifiers helping in digestion of lipids. Bile acids are also signaling molecules, which act, among other things, on lipid metabolism and immune responses, through several nuclear and membrane receptors in hepatocytes, enterocytes and cells of the immune system. Gut microbiota homeostasis also seems to be affected, directly and indirectly, by bile acid metabolism and signaling. This review summarizes recent advances in the field of bile acid signaling, studies of inflamed gut microbiome, and the therapeutic potential of bile acids in the context of inflammatory bowel disease. MDPI 2021-08-23 /pmc/articles/PMC8396648/ /pubmed/34445800 http://dx.doi.org/10.3390/ijms22169096 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Bromke, Mariusz A.
Krzystek-Korpacka, Małgorzata
Bile Acid Signaling in Inflammatory Bowel Disease
title Bile Acid Signaling in Inflammatory Bowel Disease
title_full Bile Acid Signaling in Inflammatory Bowel Disease
title_fullStr Bile Acid Signaling in Inflammatory Bowel Disease
title_full_unstemmed Bile Acid Signaling in Inflammatory Bowel Disease
title_short Bile Acid Signaling in Inflammatory Bowel Disease
title_sort bile acid signaling in inflammatory bowel disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8396648/
https://www.ncbi.nlm.nih.gov/pubmed/34445800
http://dx.doi.org/10.3390/ijms22169096
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