沙门氏菌感染引发肉鸡肠粘膜功能受损，导致器官伤甚至死亡，严重危害家禽的健康养殖。研究表明，原儿茶酸可调节肠粘膜免疫功能，抵御小鼠沙门氏菌感染，并介导自噬反应。但原儿茶酸抵御黄羽肉鸡沙门氏菌感染的作用，及其调控肠粘膜免疫功能、自噬反应的相关分子机理尚未见报道。基于此，本项目拟通过沙门氏菌感染模型，在肉鸡上验证原儿茶酸抵御沙门氏菌感染作用，研究其对肠粘膜免疫和自噬反应的影响，并利用蛋白质组学、Western Blot等方法探明其所介导的自噬信号通路，揭示基于肠粘膜免疫原儿茶酸抵御沙门氏菌感染的分子机理，为其在肉鸡养殖中的科学应用提供理论依据。

Salmonella infection causes damage to intestinal mucosal function of broilers, leading to organ injury and even death, which seriously endangers the healthy breeding of poultry. Researches showed that protocatechuic acid regulated intestinal mucosal immunity and played a significant role against Salmonella infection in mice. Furthermore, it effectively mediated the autophagy. However, the effect of protocatechuic acid against Salmonella infection in broilers and deep molecular mechanism in which it regulates intestinal mucosal immunity and autophagy have not yet been reported. Based on the above, this project intends to verify the effect of protocatechuic acid against Salmonella infection on broilers using oral infection model. Then we will study the effects on mucosal immunity and autophagy, and finally analyze the autophagy signaling pathways mediated by protocatechuic acid using proteomics and Western Blot, in order to clarify the molecular mechanism of protocatechuic acid against Salmonella infection based on intestinal mucosal immunity, and to provide theoretical basis for scientific application in broiler breeding.