Immunological mechanisms of inflammatory diseases caused by gut microbiota dysbiosis: A review
- PMID: 37311282
- DOI: 10.1016/j.biopha.2023.114985
Immunological mechanisms of inflammatory diseases caused by gut microbiota dysbiosis: A review
Abstract
The gut microbiota is indispensable for maintaining host health by enhancing the host's digestive capacity, safeguarding the intestinal epithelial barrier, and preventing pathogen invasion. Additionally, the gut microbiota exhibits a bidirectional interaction with the host immune system and promotes the immune system of the host to mature. Dysbiosis of the gut microbiota, primarily caused by factors such as host genetic susceptibility, age, BMI, diet, and drug abuse, is a significant contributor to inflammatory diseases. However, the mechanisms underlying inflammatory diseases resulting from gut microbiota dysbiosis lack systematic categorization. In this study, we summarize the normal physiological functions of symbiotic microbiota in a healthy state and demonstrate that when dysbiosis occurs due to various external factors, the normal physiological functions of the gut microbiota are lost, leading to pathological damage to the intestinal lining, metabolic disorders, and intestinal barrier damage. This, in turn, triggers immune system disorders and eventually causes inflammatory diseases in various systems. These discoveries provide fresh perspectives on how to diagnose and treat inflammatory diseases. However, the unrecognized variables that might affect the link between inflammatory illnesses and gut microbiota, need further studies and extensive basic and clinical research will still be required to investigate this relationship in the future.
Keywords: Dysbiosis; Gut microbiota; Immune disorders; Inflammatory diseases; Microbiota-gut-brain axis.
Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no conflict of interest and consent for publication. This study was funded by Jilin Provincial Department of Science and Technology, China (Grant No. 20230101163JC). The authors confirm independence from the sponsors; the content of the article has not been influenced by the sponsors.
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