Early-life antibiotic dysbiosis impairs microbial tryptophan- nicotinic acid metabolism exacerbating food allergy in adulthood
- Int Immunopharmacol. 2025 Jun 26:159:114888. doi: 10.1016/j.intimp.2025.114888.
- 1. Department of Pediatric Allergy and Immunology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou City 325000, China.
- 2. Zhejiang Chinese Medical University, Hangzhou City 310053, China.
- 3. Wenzhou Medical University, Wenzhou City 325000, China.
- 4. Department of Pediatric Allergy and Immunology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou City 325000, China. Electronic address: [email protected].
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.