Dietary tryptophan ameliorates metalaxyl-induced colitis by restoring microbial tryptophan metabolism and aryl hydrocarbon receptor activation
Exposure to metalaxyl induced low-grade colonic inflammation in wild-type mice and triggered severe colitis in IBD-susceptible mice. Integrated multi-omics analysis combining microbiome and metabolome profiling with machine learning revealed that metalaxyl exposure significantly disrupted gut microbial composition, reduced the synthesis of endogenous tryptophan-derived metabolites, inhibited aryl hydrocarbon receptor (AhR) signaling, and ultimately initiated intestinal barrier dysfunction and inflammatory cascades. Notably, dietary tryptophan restored gut tryptophan metabolite levels and strengthened AhR signaling, mitigating intestinal inflammation and repairing barrier defects.
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