Gut microbiota-driven IL-17/PPAR axis mediates epigallocatechin-induced intestinal repair in weaned lambs

Early weaning is a key strategy to improve lamb production efficiency; however, it inevitably compromises intestinal barrier integrity and function. This study aimed to investigate the effects of epigallocatechin (EGC) on growth performance and intestinal barrier function in weaned lambs, using metagenomics, metabolomics, and intestinal transcriptomics to elucidate the underlying mechanisms.

Weaning induced oxidative stress, inflammation, and metabolic disruptions in the jejunum. Supplementation with 12.5 mg/kg EGC (LE) significantly improved growth performance, reduced diarrhea incidence (P < 0.05), enhanced mucosal antioxidant capacity (P < 0.001), and strengthened anti-inflammatory ability (P < 0.001). Metagenomic analysis showed that the LE intervention enriched Ruminococcus spp. and reduced the abundance of Slackia. This microbial shift was associated with elevated luminal concentrations of valeric acid and microbial metabolites derived from EGC. Transcriptomic profiling revealed that the intervention upregulated the PPAR signaling pathway, which supports nutrient metabolism and barrier repair. Concurrently, it attenuated aberrant IL-17 signaling and promoted the restoration of mucosal immune homeostasis, indicating a resolution of excessive inflammatory responses.

Supplementation with 12.5 mg/kg EGC alleviates weaning stress by fostering a beneficial gut microbiota and promoting the production of specific metabolites. These changes reactivate PPAR mediated epithelial repair and dampen pathological immune activation. Low-dose EGC is an effective nutritional strategy to improve intestinal health and growth in weaned ruminants.