Microbiota-Mediated Immune Regulation in Atherosclerosis
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 i...
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2021-01-01
|
| Series: | Molecules |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1420-3049/26/1/179 |
| _version_ | 1797542773601075200 |
|---|---|
| author | Sahar Eshghjoo Arul Jayaraman Yuxiang Sun Robert C. Alaniz |
| author_facet | Sahar Eshghjoo Arul Jayaraman Yuxiang Sun Robert C. Alaniz |
| author_sort | Sahar Eshghjoo |
| collection | DOAJ |
| description | 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-<i>N</i>-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. |
| first_indexed | 2024-03-10T13:35:15Z |
| format | Article |
| id | doaj.art-daa0da2d59f442d7acd16dcba7017daf |
| institution | Directory Open Access Journal |
| issn | 1420-3049 |
| language | English |
| last_indexed | 2024-03-10T13:35:15Z |
| publishDate | 2021-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Molecules |
| spelling | doaj.art-daa0da2d59f442d7acd16dcba7017daf2023-11-21T07:40:13ZengMDPI AGMolecules1420-30492021-01-0126117910.3390/molecules26010179Microbiota-Mediated Immune Regulation in AtherosclerosisSahar Eshghjoo0Arul Jayaraman1Yuxiang Sun2Robert C. Alaniz3Department of Microbial Pathogenesis and Immunology, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USAArtie McFerrin Department of Chemical Engineering, Texas A&M University, College Station, TX 77840, USADepartment of Nutrition, Texas A&M University, College Station, TX 77843, USADepartment of Microbial Pathogenesis and Immunology, College of Medicine, Texas A&M University Health Science Center, Bryan, TX 77807, USAThere 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-<i>N</i>-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.https://www.mdpi.com/1420-3049/26/1/179microbiotaatherosclerosisinnate immunitymicrobiome metabolitesmacrophage |
| spellingShingle | Sahar Eshghjoo Arul Jayaraman Yuxiang Sun Robert C. Alaniz Microbiota-Mediated Immune Regulation in Atherosclerosis Molecules microbiota atherosclerosis innate immunity microbiome metabolites macrophage |
| title | Microbiota-Mediated Immune Regulation in Atherosclerosis |
| title_full | Microbiota-Mediated Immune Regulation in Atherosclerosis |
| title_fullStr | Microbiota-Mediated Immune Regulation in Atherosclerosis |
| title_full_unstemmed | Microbiota-Mediated Immune Regulation in Atherosclerosis |
| title_short | Microbiota-Mediated Immune Regulation in Atherosclerosis |
| title_sort | microbiota mediated immune regulation in atherosclerosis |
| topic | microbiota atherosclerosis innate immunity microbiome metabolites macrophage |
| url | https://www.mdpi.com/1420-3049/26/1/179 |
| work_keys_str_mv | AT sahareshghjoo microbiotamediatedimmuneregulationinatherosclerosis AT aruljayaraman microbiotamediatedimmuneregulationinatherosclerosis AT yuxiangsun microbiotamediatedimmuneregulationinatherosclerosis AT robertcalaniz microbiotamediatedimmuneregulationinatherosclerosis |