Exploration of gut microbiome and inflammation: A review on key signalling pathways.
Autor: | Nigam M; Department of Biochemistry, Hemvati Nandan Bahuguna Garhwal University, Srinagar Garhwal 246174, Uttarakhand, India. Electronic address: m.nigam@hnbgu.ac.in., Devi K; Department of Biochemistry, Hemvati Nandan Bahuguna Garhwal University, Srinagar Garhwal 246174, Uttarakhand, India., Coutinho HDM; Department of Biological Chemistry, Regional University of Cariri, Crato, Brazil. Electronic address: hdmcoutinho@gmail.com., Mishra AP; Department of Pharmacology, University of Free State, Bloemfontein 9300, South Africa. Electronic address: Mishra.ap@ufs.ac.za. |
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Jazyk: | angličtina |
Zdroj: | Cellular signalling [Cell Signal] 2024 Jun; Vol. 118, pp. 111140. Date of Electronic Publication: 2024 Mar 16. |
DOI: | 10.1016/j.cellsig.2024.111140 |
Abstrakt: | The gut microbiome, a crucial component of the human system, is a diverse collection of microbes that belong to the gut of human beings as well as other animals. These microbial communities continue to coexist harmoniously with their host organisms and perform various functions that affect the host's general health. Each person's gut microbiota has a unique makeup. The gut microbiota is well acknowledged to have a part in the local as well as systemic inflammation that underlies a number of inflammatory disorders (e.g., atherosclerosis, diabetes mellitus, obesity, and inflammatory bowel disease).The gut microbiota's metabolic products, such as short-chain fatty acids (butyrate, propionate, and acetate) inhibit inflammation by preventing immune system cells like macrophages and neutrophils from producing pro-inflammatory factors, which are triggered by the structural elements of bacteria (like lipopolysaccharide). The review's primary goal is to provide comprehensive and compiled data regarding the contribution of gut microbiota to inflammation and the associated signalling pathways. Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (Copyright © 2024 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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