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Background Neonatal necrotizing enterocolitis (NEC) is a life-threatening neonatal disease characterized by severe intestinal mucosal injury. The aryl hydrocarbon receptor (AhR) is a key regulator of intestinal homeostasis, and studies have shown that indole-3-acetic acid (IAA) can activate AhR, thereby exerting a protective effect in intestinal inflammatory diseases. However, the therapeutic potential of specific probiotic-derived metabolites in NEC prevention remains unexplored. Methods This study aims to investigate whether IAA derived from Bifidobacterium longum can alleviate the progression of NEC by activating AhR. Bifidobacterium longum BX06 (B. longum BX06) was screened from neonatal feces based on IAA production and pathogen inhibition capacity. To evaluate the prophylactic efficacy of B. longum BX06, the neonatal rat model of NEC was established via formula feeding, hypoxia/cold stress, and lipopolysaccharide (LPS) challenge. Intestinal injury was evaluated histologically via H&E staining. Ileal IAA levels, AhR, CYP1A1 expression, and inflammatory mediators (TLR4, NF-κB, IL-1β, TNF-α) were quantified using ELISA, RT-qPCR, and Western blot.Results In vitro, B. longum BX06 exhibited robust IAA synthesis and pathogen inhibition capabilities. In vivo, B. longum BX06 intervention markedly mitigated severe intestinal damage and restored depleted ileal IAA levels in NEC rats. B. longum BX06 significantly upregulated intestinal AhR and CYP1A1 expression, with ileal IAA abundance positively correlating with CYP1A1 mRNA levels. Concurrently, B. longum BX06 effectively suppressed the TLR4/NF-κB inflammatory cascade and downstream pro-inflammatory cytokines (IL-1β, TNF-α).Conclusions B. longum BX06 mitigates NEC-induced intestinal injury by activating AhR through IAA production, thereby modulating TLR4-mediated inflammatory responses. This specific metabolite-driven screening strategy provides a novel perspective for the evidence-based prevention and treatment of NEC.