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Tytuł pozycji:

Microbiota-Mediated Immune Regulation in Atherosclerosis.

Tytuł:
Microbiota-Mediated Immune Regulation in Atherosclerosis.
Autorzy:
Eshghjoo S; Department of Microbial Pathogenesis and Immunology, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA.
Jayaraman A; Artie McFerrin Department of Chemical Engineering, Texas A&M University, College Station, TX 77840, USA.
Sun Y; Department of Nutrition, Texas A&M University, College Station, TX 77843, USA.
Alaniz RC; Department of Microbial Pathogenesis and Immunology, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USA.
Źródło:
Molecules (Basel, Switzerland) [Molecules] 2021 Jan 01; Vol. 26 (1). Date of Electronic Publication: 2021 Jan 01.
Typ publikacji:
Journal Article; Review
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, c1995-
MeSH Terms:
Atherosclerosis*/immunology
Atherosclerosis*/metabolism
Atherosclerosis*/microbiology
Atherosclerosis*/pathology
Foam Cells*/immunology
Foam Cells*/metabolism
Foam Cells*/pathology
Indican*/immunology
Indican*/metabolism
Methylamines*/immunology
Methylamines*/metabolism
Gastrointestinal Microbiome/*immunology
Animals ; Basic Helix-Loop-Helix Transcription Factors/immunology ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/microbiology ; Inflammation/pathology ; Receptors, Aryl Hydrocarbon/immunology ; Receptors, Aryl Hydrocarbon/metabolism
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Grant Information:
DK118334 United States NH NIH HHS; R01AI110642 United States NH NIH HHS
Contributed Indexing:
Keywords: atherosclerosis; innate immunity; macrophage; microbiome metabolites; microbiota
Substance Nomenclature:
0 (AHR protein, human)
0 (Basic Helix-Loop-Helix Transcription Factors)
0 (Methylamines)
0 (Receptors, Aryl Hydrocarbon)
FLD0K1SJ1A (trimethyloxamine)
N187WK1Y1J (Indican)
Entry Date(s):
Date Created: 20210106 Date Completed: 20210408 Latest Revision: 20210408
Update Code:
20240105
PubMed Central ID:
PMC7795654
DOI:
10.3390/molecules26010179
PMID:
33401401
Czasopismo naukowe
There is a high level of interest in identifying metabolites of endogenously produced or dietary compounds generated by the gastrointestinal (GI) tract microbiota, and determining the functions of these metabolites in health and disease. There is a wealth of compelling evidence that the microbiota is linked with many complex chronic inflammatory diseases, including atherosclerosis. Macrophages are key target immune cells in atherosclerosis. A hallmark of atherosclerosis is the accumulation of pro-inflammatory macrophages in coronary arteries that respond to pro-atherogenic stimuli and failure of digesting lipids that contribute to foam cell formation in atherosclerotic plaques. This review illustrates the role of tryptophan-derived microbiota metabolites as an aryl hydrocarbon receptor (AhR) ligand that has immunomodulatory properties. Also, microbiota-dependent trimethylamine- N -oxide (TMAO) metabolite production is associated with a deleterious effect that promotes atherosclerosis, and metabolite indoxyl sulfate has been shown to exacerbate atherosclerosis. Our objective in this review is to discuss the role of microbiota-derived metabolites in atherosclerosis, specifically the consequences of microbiota-induced effects of innate immunity in response to atherogenic stimuli, and how specific beneficial/detrimental metabolites impact the development of atherosclerosis by regulating chronic endotoxemic and lipotoxic inflammation.
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