생화학분자생물학회입니다.
Regulation of Common Neurological Disorders by Gut Microbial Metabolites
작성자
Chang H. Kim작성일자
2022-03-24조회수
361Chang H. Kim( chhkim@umich.edu ) | ||
2017-present | Professor, Department of Pathology, University of Michigan, USA | |
2017-present | Betz Endowed Professor, Mary H Weiser Food Allergy Center, University of Michigan, USA | |
2002-2017 | Assistant, Associate and Full Professor, Department of Pathobiology, Purdue University, USA | |
1999-2002 | Postdoctoral fellow, Department of Pathobiology, Stanford University, USA | |
1995-1998 | PhD, Department of Microbiology and Immunology, Indiana University, USA | |
1986-1992 | BS, MS, Department of Biology/Biological Engineering, KAIST, Korea |
Regulation of Common Neurological Disorders by Gut Microbial Metabolites
The gut is connected to the CNS by immunological mediators, lymphocytes, neurotransmitters, microbes and microbial metabolites. A mounting body of evidence indicates that the microbiome exerts significant effects on immune cells and CNS cells. These effects frequently result in the suppression or exacerbation of inflammatory responses, the latter of which can lead to tissue damage, altered synapse formation and disrupted maintenance of the CNS. Herein, we review recent progress in research on the microbial regulation of CNS diseases with a focus on major gut microbial metabolites, such as short-chain fatty acids, tryptophan metabolites, and secondary bile acids. Pathological changes in the CNS are associated with dysbiosis and altered levels of microbial metabolites, which can further exacerbate various neurological disorders. The cellular and molecular mechanisms by which these gut microbial metabolites regulate inflammatory diseases in the CNS are discussed. We highlight the similarities and differences in the impact on four major CNS diseases, i.e., multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and autism spectrum disorder, to identify common cellular and molecular networks governing the regulation of cellular constituents and pathogenesis in the CNS by microbial metabolites.
Experimental & Molecular Medicine (2021) 53:1821–1833
https://doi.org/10.1038/s12276-021-00703-x