Early-Life Gut Dysbiosis: A Driver of Later-Life Fibrosis?

Abstract

Using a novel mouse model of scleroderma induced by immunization with topoisomerase-I peptide-loaded dendritic cells, Mehta et al. found that early-life antibiotic exposure resulted in increased later-life fibrosis in the skin and lungs. These observations advance the novel concept that gut microbiome alterations caused by early-life exposures may contribute to scleroderma pathogenesis, and warrant in-depth characterization and validation in complementary disease models.