Early-life antibiotic exposure is a significant environmental risk factor for food allergy(FA), yet its pathogenic mechanisms remain unclear. This study , utilizing an early-life antibiotic exposure FA mice model, aryl hydrocarbon receptor (AhR) knockout mice, and an in vitro intestinal epithelial injury model, systematically elucidates the critical role of the "microbiota–tryptophan metabolism–AhR–ILC3–IL-22–gut barrier" axis. The results demonstrate that early-life antibiotic exposure leads to gut microbiota dysbiosis and a reduction in the tryptophan metabolite indole-3-carboxaldehyde (Iald), which subsequently suppresses AhR signaling, decreases intestinal group 3 innate lymphoid cell (ILC3) proportions and interleukin-22 (IL-22) secretion, ultimately impairing gut barrier function and increasing susceptibility to FA. Exogenous IAld supplementation significantly restored ILC3–IL-22 axis function, enhanced intestinal epithelial tight junction protein expression, and alleviated allergic symptoms, effects that were entirely AhR-dependent. Mechanistically , IAld promotes barrier-related protein expression in intestinal epithelial cells directly via AhR activation and synergistically enhances barrier repair through the ILC3–IL-22 pathway .