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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Complement System in Alcohol-Associated Liver Disease

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Author(s):
Santiesteban-Lores, Lazara Elena [1] ; Carneiro, Milena Carvalho [1] ; Isaac, Lourdes [1] ; Bavia, Lorena [1]
Total Authors: 4
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Sao Paulo, SP - Brazil
Total Affiliations: 1
Document type: Review article
Source: Immunology Letters; v. 236, p. 37-50, AUG 2021.
Web of Science Citations: 0
Abstract

Innate immunity contributes effectively to the development of Alcohol-Associated liver disease (ALD). Particularly, human studies and murine models of ALD have shown that Complement activation plays an important role during the initial and later stages of ALD. The Complement System may contribute to the pathogenesis of this disease since it has been shown that ethanol-derived metabolic products activate the Complement cascade on liver membranes, leading to hepatocellular damage. However, studies evaluating the plasma levels of Complement proteins in ALD patients present contradictory results in some cases, and do not establish a well-marked role for each Complement component. The impairment of leukocyte chemoattractant activity observed in these patients may contribute to the susceptibility to bacterial infections in the latter stages of the disease. On the other hand, murine models of ALD have provided more detailed insights into the mechanisms that link the Complement System to the pathogenesis of the disease. It has been observed that Classical pathway can be activated via C1q binding to apoptotic cells in the liver and contributes to the development of hepatic inflammation. C3 contributes to the accumulation of triglycerides in the liver and in adipose tissue, while C5 seems to be involved with inflammation and liver injury after chronic ethanol consumption. In this review, we present a compendium of studies evaluating the role of Complement in human and murine models of ALD. We also discuss potential therapies to human ALD, highlighting the use of Complement inhibitors. (AU)

FAPESP's process: 17/12924-3 - Etiopathogenesis of Leptospirosis: contribution of the complement system for the control of infection in vivo and in vitro and inflammatory response: identification of gene polymorphisms of the complement system in Leptospirosis patients
Grantee:Lourdes Isaac
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 19/19800-3 - Training in microbiology and immunology techniques
Grantee:Milena Carvalho Carneiro
Support Opportunities: Scholarships in Brazil - Technical Training Program - Technical Training
FAPESP's process: 07/03393-2 - Component C5 dependent gene expression in mice ethanol-induced liver injury
Grantee:Lorena Bavia
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)