Antibiotics drive microbial imbalance and vitiligo development in mice.

Abstract

Vitiligo is impacted by environmental triggers. We studied the contribution of the microbiome in FH mice, where depigmentation is mediated by tyrosinase-reactive T cells. Mice received oral antibiotics and were monitored for depigmentation. The microbiome was studied in fecal and skin samples by 16S rRNA analysis. Resulting T-cell distributions were evaluated. In untreated mice, pigment loss did not expand to the pelage, whereas mice in the ampicillin group were about 1/3 depigmented at 30 weeks. Contrary to models of autoimmunity that are less dependent on IFN-γ, ampicillin but not neomycin treatment correlated with accelerated disease and reduced bacteria in fecal pellets. Modified cytokine patterns in tissue and serum suggest a response that transcends the gut. Ampicillin-induced depigmentation was accompanied by gut but not skin dysbiosis, and reduced T cells in both sites. Neomycin induced a redistribution of gut T cells and accumulation of skin Tregs. This treatment spurred a Bacteroides-dominated population of fecal bacteria. Reduced diversity is prominent especially after ampicillin treatment, when the gut is dominated by Pseudomonas species. In line with current concepts relating the microbiome and the immune system, we predict that dietary measures might promote skin health and delay vitiligo onset.