Early-life antibiotic dysbiosis impairs microbial tryptophan- nicotinic acid metabolism exacerbating food allergy in adulthood

Food allergy (FA) pathogenesis links to intestinal dysbiosis, with antibiotic exposure a suspected risk factor, yet mechanisms are unclear. Our study shows early life (EL) antibiotic exposure in mice heightens susceptibility to OVA - induced allergic intestinal inflammation. EL - antibiotics cause intestinal dysbiosis, like Clostridia and Muribaculaceae depletion and Sutterellaceae enrichment, disrupting tryptophan metabolism and reducing nicotinic acid (NA). NA deficiency impairs gut barrier and Th2/Treg balance. However, NA supplementation restores these via GPR109A. In human pediatric cohorts, food - allergic children with EL - antibiotic exposure have lower gut NA levels. We integrated mouse and human data with multi - omics, revealing EL - Abx regulates FA through the "microbiota - metabolism - immunity" axis, and suggest targeting NA pathway to counter antibiotic - related FA risk.