Escherichia Abundance and Metabolism Align with Vitiligo Disease Activity.

Zhussipbek Mukhatayev, Artur Kovenskiy, Ziyou Ren, Stephanie M Rangel, Nurlubek Katkenov, Yerkhanat Khuanbai, Rohan Shivde, Moriel Daniel, Emilia R Dellacecca, Kettil Cedercreutz, Yekaterina Ostapchuk, Ayaulum Nurgozhina, Laura Chulenbayeva, Madiyar Nurgaziyev, Zharkyn Jarmukhanov, Marzhan Nurlankyzy, Kamilya Kozhdan, Symbat Seidulla, Zhanel Mukhanbetzhanova, Shynggyss Sergazy, Samat Kozhakhmetov, Yasmeen Ali, Karishma M Daftary, Stefan J Green, Roopal V Kundu, Almagul Kushugulova, I Caroline Le Poole
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Abstract

Vitiligo is a cutaneous autoimmune disorder characterized by progressive depigmentation due to melanocyte destruction by cytotoxic T cells. Genetic factors predispose patients to the disease and are supported by environmental factors that often initiate new disease episodes. We investigated whether disease outcomes were partially defined by pathogenic microbes that drive nutrient deficiency and inflammation. Our study presents the results of research on the diet and gut microbiome composition of patients with vitiligo and healthy controls from Kazakhstan and the United States. Dietary nutrient intake was assessed using the National Institutes of Health-generated Diet History Questionnaire. Patients with active vitiligo exhibit a limited intake of specific fatty acids, amino acids, fiber, and zinc. Disease activity was further characterized by the abundance of Odoribacter and Escherichia in the gut. Metabolic pathway analysis supported the role of the Escherichia genus in disease activity by limiting energy metabolism and amino acid biosynthetic pathways. Disease activity was also associated with elevated circulating proinflammatory cytokines. These findings suggest that nutritional limitations are not compensated by metabolites from the gut microbiome in active disease, potentially leaving room for inflammation and exacerbating vitiligo. The intricate relationship among diet, gut microbiome composition, and disease progression in vitiligo highlights potential avenues for targeted interventions to reduce autoimmune activity and improve patient outcomes.

白癜风是一种皮肤自身免疫性疾病,其特征是黑色素细胞被细胞毒性 T 细胞破坏而导致进行性色素脱失。遗传因素使患者易患此病,而环境因素往往会引发新的疾病发作。我们质疑疾病的结果是否部分取决于导致营养缺乏和炎症的致病微生物。我们的研究展示了来自哈萨克斯坦和美国的白癜风患者和健康对照组的饮食和肠道微生物组组成的研究结果。我们使用美国国立卫生研究院(NIH)制作的饮食史问卷对饮食营养摄入量进行了评估。病情活跃的白癜风患者表现出特定脂肪酸、氨基酸和锌的摄入量有限。疾病活动的进一步特征是肠道中存在大量的奥德菌属和埃希氏菌属。代谢途径分析支持埃希氏菌属通过限制能量代谢和氨基酸生物合成途径在疾病活动中发挥作用。疾病活动还与循环促炎细胞因子的升高相一致。这些研究结果表明,在疾病活跃期,肠道微生物组的代谢产物无法弥补营养的限制,从而有可能为炎症留下空间并加剧白癜风。白癜风患者的饮食、肠道微生物组组成和疾病进展之间错综复杂的关系凸显了有针对性的干预措施以减少自身免疫活动和改善患者预后的潜在途径。
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