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Mini-Reviews in Medicinal Chemistry

Editor-in-Chief

ISSN (Print): 1389-5575
ISSN (Online): 1875-5607

Review Article

The Role of Gut Microbiota in Inflammatory Bowel Disease-Current State of the Art

Author(s): Hassan Askari, Sara Shojaei-Zarghani, Ehsan Raeis-Abdollahi, Hossein Kargar Jahromi, ‪Payman Raise Abdullahi, Karim Daliri, Amir Tajbakhsh, Leila Rahmati and Ali Reza Safarpour*

Volume 23, Issue 13, 2023

Published on: 21 October, 2022

Page: [1376 - 1389] Pages: 14

DOI: 10.2174/1389557522666220914093331

Open Access Journals Promotions 2
Abstract

The human microbiome comprises the genomes of the microbiota that live on and within humans, such as protozoa, archaea, eukaryotes, viruses, and most bacteria. Gastrointestinal disorders such as inflammatory bowel disease, colon cancer, celiac disease, and irritable bowel syndrome can all be triggered by a change in gut flora. The alteration of the gut microbiota (also known as "gut dysbiosis") is affected by host genetics, nutrition, antibiotics, and inflammation, and it is associated with the development of inflammatory bowel disease (IBD). Also, intestinal epithelial dysfunction, altered autophagy, and immune hyperactivation are frequently detected in individuals with severe IBD, which may be attributed to impaired miRNA expression functions. While the exact mechanisms of how Gut Microbiota may cause IBD and intestinal epithelial dysfunction are still debated, recent data point toward the possibility that hormones, gender and miRNAs expression are modifiable contributors to IBD. This review summarizes the current evidence for an association between hormones, gender and miRNAs and Gut Microbiota in IBD and discusses potential mechanisms by which gut microbiota may impact IBD. The study also outlines critical unanswered topics that need to be solved to enhance IBD prevention and treatment in people with gut dysbiosis.

Keywords: Inflammatory bowel disease, ulcerative colitis, crohn's disease, gut, microbiota, pathogenesis, gut dysbiosis.

Graphical Abstract
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