Gençer Bingöl Feray, Kocyigit Emine, Çelik Elif, Ağagündüz Duygu, Budán Ferenc
Department of Nutrition and Dietetics, Faculty of Health Sciences, Burdur Mehmet Akif Ersoy University, Burdur 15100, Türkiye.
Department of Nutrition and Dietetics, Faculty of Health Sciences, Ordu University, Ordu 52200, Türkiye.
Int J Mol Sci. 2025 Jun 7;26(12):5464. doi: 10.3390/ijms26125464.
Multiple Sclerosis (MS) is a chronic disease with autoimmune and neurodegenerative features that affect the nervous system. Genetic predisposition and environmental factors, such as vitamin D deficiency and dysbiosis activating a pro-inflammatory response, have a role in the etiology of the disease. In this context, the interactions of vitamin D with the gut microbiota and immune system have attracted attention in recent years. Vitamin D (1,25-dihydroxycholecalciferol) modulates the immune response by binding to the Vitamin D receptor (VDR). This pathway supports the functions of regulatory T cells by suppressing the activity of T helper cells 1 and 17 (Th1 and Th17). In MS patients, dysbiosis is characterized by a decrease in microbial diversity, and an increase in pro-inflammatory species is observed when compared to healthy individuals. Vitamin D has protective effects on eubiosis via VDR in intestinal epithelial cells, also reducing intestinal permeability by regulating tight junction proteins. In this way, vitamin D may contribute to the prevention of systemic inflammation. Although the relationship between vitamin D and the immune system is well documented, studies that address the triad of vitamin D level, gut microbiota, and immune response in MS are still limited.
多发性硬化症（MS）是一种具有自身免疫和神经退行性特征的慢性疾病，会影响神经系统。遗传易感性和环境因素，如维生素D缺乏和激活促炎反应的微生物群落失调，在该疾病的病因中起作用。在这种背景下，近年来维生素D与肠道微生物群和免疫系统的相互作用引起了关注。维生素D（1,25-二羟基胆钙化醇）通过与维生素D受体（VDR）结合来调节免疫反应。该途径通过抑制辅助性T细胞1和17（Th1和Th17）的活性来支持调节性T细胞的功能。在MS患者中，微生物群落失调的特征是微生物多样性降低，与健康个体相比，促炎物种增加。维生素D通过肠道上皮细胞中的VDR对正常微生物群落具有保护作用，还通过调节紧密连接蛋白来降低肠道通透性。通过这种方式，维生素D可能有助于预防全身炎症。尽管维生素D与免疫系统之间的关系已有充分记录，但针对MS中维生素D水平、肠道微生物群和免疫反应三者关系的研究仍然有限。
