Gut Acidification Impairment Links Commensal Decline to Infantile Eczema：A cross-sectional study

Abstract The infant gut microbiota is essential for immune development, yet its disruption in eczema remains poorly understood. In this cross-sectional study, we compared the gut microbiota and fecal metabolites of infants with eczema and healthy controls, and used in vitro fermentation to assess microbial metabolic activity. Infants with eczema showed reduced levels of acidogenic and acidophilic bacteria—including Enterococcus faecium, Citrobacter, and Streptococcus unclassified—along with impaired intestinal acidification, altered short-chain fatty acid profiles, and decreased Lactobacillus counts and bile acid levels.Based on these findings, we propose a Dual Driving Force Hypothesis of infant gut microbiota succession. In this model, early lactate accumulation acts as the primary ecological driver, fostering colonization by acid-tolerant commensals and enabling Lactobacillus-mediated bile acid maturation as a secondary driver. The acidophilic bacteria that thrive in this lactate-enriched environment likely serve as immune stimuli, promoting the postnatal shift from TH2- to TH1-skewed immunity.Excessive hygiene may reduce environmental microbial exposure, delay microbial succession, and impair immune programming, thereby increasing eczema risk. Our results offer mechanistic support for the hygiene hypothesis and point toward microbiome-based strategies for early prevention of immune-mediated conditions like eczema.