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REVIEW article
Front. Gastroenterol.
Sec. Gastrointestinal Infection
Volume 3 - 2024 |
doi: 10.3389/fgstr.2024.1452430
Innate Immune Cells in the Pathogenesis of Inflammatory Bowel Disease - From Microbial Metabolites to Immune Modulation
Provisionally accepted- 1 University of Pavia, Pavia, Lombardy, Italy
- 2 University of Milano-Bicocca, Milan, Lombardy, Italy
- 3 University of Cambridge, Cambridge, United Kingdom
Inflammatory Bowel Disease (IBD) is a term used to describe a group of disorders characterised by chronic inflammation of the gastrointestinal tract, with Crohn's Disease (CD) and Ulcerative Colitis (UC) being the most common. While still not fully understood, pathogenesis is believed to be multifactorialthe result of an interplay between genetic susceptibility, immune dysregulation and environmental factors that all lead to chronic inflammation and tissue remodelling.Innate immune cells, which orchestrate the initial defence mechanisms and modulate the subsequent immune response, play a central role in disease initiation and progression. This review examines the complex involvement of innate immune cells in IBD, emphasizing their interactions with environmental factors and the gut microbiome.We highlight the importance of microbial dysbiosis and impaired intestinal barrier function in disease pathogenesis, and the role that innate immune cells play not only as first responders, but also as key players in maintaining intestinal barrier integrity and gut microbiome.This review provides a comprehensive summary of the role that innate immune cells play in IBD pathogenesis with emphasis on the increasingly recognized role of the gut microbiome. A better understanding of innate immune cell mechanisms and of microbiome-immune interactions is key for the development of novel targeted therapies.
Keywords: IBD - inflammatory bowel disease, Macrophages, Innate lymphocyte cells (ILCs), short chain fatty acid (SCFA), Crohns disease, ulcerative colitis, Neutrophils, Innate immunity
Received: 20 Jun 2024; Accepted: 11 Nov 2024.
Copyright: © 2024 Mousa, Invernizzi and Mousa. 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) or licensor 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.
* Correspondence:
Hani S. Mousa, University of Cambridge, Cambridge, United Kingdom
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