Haiping Xu, Yantian Tang, Siyu Zhang, Guosheng Wang
Escherichia coli (E. coli)-induced enteritis impairs intestinal barrier function, immune homeostasis, and growth performance in broilers. This study investigated whether dietary curcumin alleviates E. coli-induced intestinal injury by modulating macrophage-mediated inflammatory responses through the p38 MAPK signaling pathway. Broilers were fed either a basal or curcumin-supplemented diet and challenged with E. coli. Growth performance, intestinal inflammatory cytokines, morphology, barrier-related gene expression, goblet cell density, and ileal macrophage responses were evaluated. Lipopolysaccharide (LPS)-stimulated HD11 cells were used to examine the underlying mechanism. Curcumin supplementation increased body weight, average daily feed intake, and average daily gain in E. coli-challenged broilers, without significantly affecting the feed conversion ratio. Curcumin also reduced jejunal and ileal IL-1β, IL-6, and TNF-α levels; improved villus morphology and the villus height-to-crypt depth ratio; and upregulated CLDN1, OCLN, ZO-1, and MUC2 expression. In addition, curcumin restored goblet cell density and ileal macrophage abundance while suppressing macrophage-derived pro-inflammatory cytokine expression. In HD11 cells, curcumin inhibited LPS-induced inflammatory cytokine expression and secretion and reduced p38 MAPK phosphorylation, whereas pharmacological activation of p38 partially reversed these effects. In conclusion, dietary curcumin alleviated E. coli-induced enteritis in broilers by suppressing intestinal inflammation, preserving intestinal barrier function, and modulating macrophage-mediated immune responses. In vitro findings further suggest that inhibition of p38 MAPK signaling may contribute to the anti-inflammatory effects of curcumin on chicken macrophages.