仔猪缺铁症是仔猪的易发病，而给仔猪补铁也已成为普遍认可和使用的常规手段。然而，在仔猪腹泻或感染应激下补铁却适得其反。由于铁是动物机体和病原体生长需要的共同营养素，争夺铁这一稀缺资源已成动物体与病原体间的一场战役。但目前对于仔猪是否通过减少游离铁来控制细菌感染的免疫作用及机制尚不清楚。本项目拟在系统阐述仔猪铁代谢与免疫功能关系的基础上，通过构建仔猪体内染菌模型和铁代谢异常模型，聚焦机体铁螯合对病原体生长的抑制调控，运用分子生物学、细胞生物学和免疫学等手段，从基因、蛋白、细胞、组织等不同层次探讨铁限制性调控对仔猪抗感染免疫的影响，并分别从细菌铁受体、铁调素和巨噬细胞角度进一步探索其调控的可能机制，为从限铁途径寻找抗菌物质提供新思路，为在感染条件下仔猪缺铁症的预防和控制提供新视角。

Iron deficiency in piglets is a susceptible nutritional deficiency disease. Iron supplementation has been proved to be beneficial and used widely in pig breeding. However, it is no work for piglets under diarrhea or infection stress. Iron is an essential nutrient for both animals and pathogens. Given the absolute requirement for iron by virtually all pathogens, an important facet of the innate immune system is to limit iron availability to invading microbes in a process termed nutritional immunity. The project will take piglets as mode animals to figure out the relationship between iron homeostasis and innate immune defense. Researches will tackle the challenging questions how the innate immune system strengthens iron-withholding defenses to response to infection, ensuring that host-pathogen interface remains an ever-evolving battleground for iron. It is possible to design therapies that manipulate the hepcidin axis to confer tolerance to infectious diseases. The results will be expected to be beneficial in treating infectious diseases that are exacerbated by iron supplementation.