Galangin ameliorates Salmonella Pullorum-induced enteritis in Danzhou chicks through gut microbiota-derived indole-3-lactic acid-mediated AHR activation.

Antibiotic restrictions in poultry production necessitate natural alternatives against Salmonella Pullorum, a pathogen causing severe enteritis and high chick mortality. We show that the dietary flavonoid galangin alleviates S. Pullorum-induced intestinal injury not via direct antimicrobial action, but by modulating gut microbiota to enrich tryptophan-derived indole-3-lactic acid (ILA). Galangin restored growth, preserved barrier integrity, reduced liver bacterial translocation, and suppressed inflammation in infected chicks. Fecal microbiota transplantation from galangin-treated donors recapitulated these benefits, confirming microbiota dependence. ILA activated the aryl hydrocarbon receptor (AHR), concurrently inhibiting NF-κB and HIF-1α pathways-key drivers of Salmonella-exploited inflammation and metabolic reprogramming-thereby enhancing mucosal defense and limiting intracellular bacterial survival. Pharmacological AHR blockade or NF-κB/HIF-1α activation abolished galangin's effects. Collectively, these findings establish that galangin acts as a prebiotic-like agent via the ILA-AHR axis, providing a mechanism-based strategy for antibiotic reduction in sustainable poultry production.