Lipopolysaccharide-induced intestinal mucosal injury disrupts proteostasis in broiler chickens

Intestinal damage induced by immune stress leads to economic losses in broiler production; however, the underlying mechanisms remain unclear. This experiment investigated the effects of immune stress on the intestinal mucosa proteome of Arbour Acres (AA) broilers challenged with <i>Escherichia coli</i> lipopolysaccharide (LPS). A total of 144 one-day-old, male, AA broiler chickens were randomly divided into two groups: the treatment group was challenged with LPS and the control group received an equal volume of saline injection. On day 42, intestinal morphology, enterocytes and mucosal proteomes were analysed from three birds in each replicate, with a total of six replicates per group. The microvilli of intestinal epithelial cells exhibited damage and necrotic enterocytes were evident in broilers challenged with LPS. Proteomic analysis indicated that 851 proteins were differentially expressed in the intestinal mucosa of broiler chickens from the immune stress group; 463 proteins were down-regulated, and 388 proteins were up-regulated. Functional analysis revealed that LPS disrupted intestinal mucosa protein homeostasis, affecting beta-oxidation of fatty acids, oxidative stress and immune function. Furthermore, immune stress increased the expression of alanine, tyrosine, leucine, isoleucine, tryptophan, arginine and serine-tRNA ligase. The data suggest that gut damage in broiler chickens induced by LPS is triggered by dysfunctional and unbalanced proteostasis alterations. This study provides new insights into the mechanisms by which immune challenges impair nutrient absorption and mucosal immunity in broiler chickens.