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. 2021 Nov;23(11):37.
doi: 10.1007/s11940-021-00693-1. Epub 2021 Oct 29.

Gut Microbiome as Potential Therapeutics in Multiple Sclerosis

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Gut Microbiome as Potential Therapeutics in Multiple Sclerosis

Wen Zhu et al. Curr Treat Options Neurol. 2021 Nov.

Abstract

Purpose of review: The gut microbiome is an emerging arena to investigate multiple sclerosis (MS) pathogenesis and potential therapeutics. In this review, we summarize the available data and postulate the feasibilities of potential MS therapeutic approaches that modulate the gut microbiome.

Recent findings: Growing evidence indicates dysbiosis in the gut bacterial ecosystem in MS. Diet and other interventions produce biologically significant changes in the gut bacterial communities and functions, can potentially regulate the immune system, and benefit people with MS. While well-conducted investigations of the therapeutic mechanisms for targeting gut microbiome in animal models and humans remain limited, promising connections between various mechanisms of gut microbiome regulation and beneficial effects on MS outcomes are emerging.

Summary: To date, studies examining the microbiome-based therapies in MS remain limited in number and follow-up duration. There is a clear need to determine the long-term efficacy and safety of these approaches, and to identify their underlying mechanisms of actions.

Keywords: Calorie restriction diet; Fecal transplantation; Ketogenic diet; Microbiome; Multiple sclerosis; Prebiotics; Probiotics.

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Conflict of interest statement

Declarations Conflict of Interest The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Putative mechanisms of action of potential microbiome-based therapeutic approaches. Microbiome-based therapeutic approaches (probiotics, prebiotics, ketogenic diet, calorie restriction, and fecal microbiota translation) could potentially modulate the immune system in MS patients through a variety of mechanisms (also see Table 1): decrease in CD14highCD16 monocytes, decrease in antigen-presenting cells, decrease in Th1 and Th17 cells as well as reduction in IL17 production, induction of C D4+CD25+FoxP3+ regulatory T cells (Tregs), and increased IL-10 expression.

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