Nemati Mohammad Hosein, Yazdanpanah Esmaeil, Kazemi Roya, Orooji Niloufar, Dadfar Sepehr, Oksenych Valentyn, Haghmorad Dariush
Student Research Committee, Semnan University of Medical Sciences, Semnan 3514799442, Iran.
Department of Immunology, School of Medicine, Semnan University of Medical Sciences, Semnan 3514799442, Iran.
Biology (Basel). 2025 Apr 17;14(4):435. doi: 10.3390/biology14040435.
Multiple sclerosis (MS) is a well-known, chronic autoimmune disorder of the central nervous system (CNS) involving demyelination and neurodegeneration. Research previously conducted in the area of the gut microbiome has highlighted it as a critical contributor to MS pathogenesis. Changes in the commensal microbiota, or dysbiosis, have been shown to affect immune homeostasis, leading to elevated levels of pro-inflammatory cytokines and disruption of the gut-brain axis. In this review, we provide a comprehensive overview of interactions between the gut microbiota and MS, especially focusing on the immunomodulatory actions of microbiota, such as influencing T-cell balance and control of metabolites, e.g., short-chain fatty acids. Various microbial taxa (e.g., and ) were suggested to lay protective roles, whereas was associated with disease aggravation. Interventions focusing on microbiota, including probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary therapies to normalize gut microbial homeostasis, suppress inflammation and are proven to improve clinical benefits in MS patients. Alterations in gut microbiota represent opportunities for identifying biomarkers for early diagnosis, disease progression and treatment response monitoring. Further studies need to be conducted to potentially address the interplay between genetic predispositions, environmental cues, and microbiota composition to get the precise mechanisms of the gut-brain axis in MS. In conclusion, the gut microbiota plays a central role in MS pathogenesis and offers potential for novel therapeutic approaches, providing a promising avenue for improving clinical outcomes in MS management.
多发性硬化症（MS）是一种众所周知的中枢神经系统（CNS）慢性自身免疫性疾病，涉及脱髓鞘和神经退行性变。先前在肠道微生物群领域进行的研究已强调其为MS发病机制的关键促成因素。共生微生物群的变化，即生态失调，已被证明会影响免疫稳态，导致促炎细胞因子水平升高和肠-脑轴破坏。在本综述中，我们全面概述了肠道微生物群与MS之间的相互作用，尤其关注微生物群的免疫调节作用，如影响T细胞平衡和控制代谢产物（如短链脂肪酸）。各种微生物分类群（如 和 ）被认为具有保护作用，而 与疾病加重相关。针对微生物群的干预措施，包括益生菌、益生元、粪便微生物群移植（FMT）以及使肠道微生物稳态正常化的饮食疗法，可抑制炎症，并已被证明能改善MS患者的临床疗效。肠道微生物群的改变为识别早期诊断、疾病进展和治疗反应监测的生物标志物提供了机会。需要进一步开展研究，以探讨遗传易感性、环境因素和微生物群组成之间的相互作用，从而明确MS中肠-脑轴的精确机制。总之，肠道微生物群在MS发病机制中起核心作用，并为新的治疗方法提供了潜力，为改善MS管理的临床结果提供了一条有前景的途径。
