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, 10⁹ 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.

随着全球变暖，热应激（HS）对养殖业的危害越来越普遍，导致动物生产性能下降，免疫力低下。本研究旨在分析HS对沙门氏菌感染鸡肠道免疫功能的影响。将 14 日龄肉鸡分为以下四组，每组 8 个重复：对照（对照）、热应激（HS）、鼠伤寒沙门氏菌（ST）和热应激+鼠伤寒沙门氏菌（HS+ST）。肉鸡在 15 至 28 日龄期间承受 35 °C 的热应激。鼠伤寒沙门氏菌 (ST, 14028, 10 ⁹在 29 日龄时通过口服给药，将 cfu/mL) 接种到 ST 组和 HS+ST 组鸡中。在鼠伤寒沙门氏菌给药后的第 4 天，在感染鼠伤寒沙门氏菌的鸡中观察到空肠 IgA 水平升高。在鼠伤寒沙门氏菌感染的肉鸡中评估了热应激对 TLR4-NFκB-NLRP3 和 TLR4-TBK1 信号传导的机制调节。热应激显着抑制细胞因子的表达，包括 TNF-α、IL-6、IL-1β、NLRP3、caspase-1、NF-κB-p65 和 p-NF-κB-p65，以及 TLR4-TBK1 细胞因子 IFN-感染鼠伤寒沙门氏菌的肉鸡空肠中的α、IFN-γ、p-IRF3和p-TBK1。集体，