دورية أكاديمية
Modulation of multiple sclerosis risk and pathogenesis by the gut microbiota: Complex interactions between host genetics, bacterial metabolism, and diet.
| العنوان: | Modulation of multiple sclerosis risk and pathogenesis by the gut microbiota: Complex interactions between host genetics, bacterial metabolism, and diet. |
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| المؤلفون: | Montgomery TL; Department of Biomedical and Health Sciences, University of Vermont, Burlington, Vermont, USA., Peipert D; Department of Biomedical and Health Sciences, University of Vermont, Burlington, Vermont, USA., Krementsov DN; Department of Biomedical and Health Sciences, University of Vermont, Burlington, Vermont, USA. |
| المصدر: | Immunological reviews [Immunol Rev] 2024 May 08. Date of Electronic Publication: 2024 May 08. |
| Publication Model: | Ahead of Print |
| نوع المنشور: | Journal Article; Review |
| اللغة: | English |
| بيانات الدورية: | Publisher: Blackwell Country of Publication: England NLM ID: 7702118 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1600-065X (Electronic) Linking ISSN: 01052896 NLM ISO Abbreviation: Immunol Rev Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: <2002-> : Oxford : Blackwell Original Publication: Copenhagen, Munksgaard. |
| مستخلص: | Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, affecting nearly 2 million people worldwide. The etiology of MS is multifactorial: Approximately 30% of the MS risk is genetic, which implies that the remaining ~70% is environmental, with a number of factors proposed. One recently implicated risk factor for MS is the composition of the gut microbiome. Numerous case-control studies have identified changes in gut microbiota composition of people with MS (pwMS) compared with healthy control individuals, and more recent studies in animal models have begun to identify the causative microbes and underlying mechanisms. Here, we review some of these mechanisms, with a specific focus on the role of host genetic variation, dietary inputs, and gut microbial metabolism, with a particular emphasis on short-chain fatty acid and tryptophan metabolism. We put forward a model where, in an individual genetically susceptible to MS, the gut microbiota and diet can synergize as potent environmental modifiers of disease risk and possibly progression, with diet-dependent gut microbial metabolites serving as a key mechanism. We also propose that specific microbial taxa may have divergent effects in individuals carrying distinct variants of MS risk alleles or other polymorphisms, as a consequence of host gene-by-gut microbiota interactions. Finally, we also propose that the effects of specific microbial taxa, especially those that exert their effects through metabolites, are highly dependent on the host dietary intake. What emerges is a complex multifaceted interaction that has been challenging to disentangle in human studies, contributing to the divergence of findings across heterogeneous cohorts with differing geography, dietary preferences, and genetics. Nonetheless, this provides a complex and individualized, yet tractable, model of how the gut microbiota regulate susceptibility to MS, and potentially progression of this disease. Thus, we conclude that prophylactic or therapeutic modulation of the gut microbiome to prevent or treat MS will require a careful and personalized consideration of host genetics, baseline gut microbiota composition, and dietary inputs. (© 2024 The Authors. Immunological Reviews published by John Wiley & Sons Ltd.) |
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| معلومات مُعتمدة: | F31NS120381 United States NS NINDS NIH HHS; R01NS097596 United States NS NINDS NIH HHS; T32AI055402-16A1 United States NS NINDS NIH HHS; P30GM118228-05S3 United States GM NIGMS NIH HHS |
| فهرسة مساهمة: | Keywords: SCFA; diet; genetics; microbiome; multiple sclerosis; tryptophan |
| تواريخ الأحداث: | Date Created: 20240508 Latest Revision: 20240508 |
| رمز التحديث: | 20240508 |
| DOI: | 10.1111/imr.13343 |
| PMID: | 38717158 |
| قاعدة البيانات: | MEDLINE |
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