Heat stress inhibits TLR4-NF-κB and TLR4-TBK1 signaling pathways in broilers infected with Salmonella Typhimurium.

With the global warming, the harm of heat stress (HS) to the breeding industry has become more common, which causes the decline of animal production performance and low immunity. This study aimed to analyze the effect of HS on the intestinal immune function of Salmonella-infected chickens. Fourteen-day-old broilers were divided into the following four groups of eight replicates: control (Control), heat stress (HS), Salmonella Typhimurium (ST), and heat stress + Salmonella Typhimurium (HS+ST). The broilers were subjected to a heat stress of 35 °C from 15 to 28 days of age. Salmonella Typhimurium (ST, 14028, 10 cfu/mL) was inoculated, via oral administration at 29 days of age, into ST and HS+ST group birds. On the 4th day after Salmonella Typhimurium administration, an increase in jejunum IgA levels was observed in chickens infected with Salmonella Typhimurium. Mechanistic regulation of TLR4-NFκB-NLRP3 and TLR4-TBK1 signaling by heat stress was evaluated in Salmonella Typhimurium-infected broilers. Heat stress markedly inhibited the expression of cytokines including TNF-α, IL-6, IL-1β, NLRP3, caspase-1, NF-κB-p65, and p-NF-κB-p65, and the TLR4-TBK1 cytokines IFN-α, IFN-γ, p-IRF3, and p-TBK1 in jejunum of broilers infected with Salmonella Typhimurium. Collectively, our results demonstrate that heat stress can inhibit intestinal immune response by downregulating the expression of TLR4-NFκB-NLRP3 and TLR4-TBK1 signaling pathways in broilers infected with Salmonella Typhimurium.