新生儿Fc受体FcRn介导的母乳IgG吸收受限是导致仔猪被动免疫低下，引起仔猪死亡的重要原因，但目前关于FcRn调控机制研究还较少报道。结合他人和本项目前期研究推测粪菌移植（FMT）可通过TLR2/4激活NF-κB通路和MARCHs调控FcRn，但其具体分子机制仍有待证明。本项目首先拟利用Transwell构建IPEC-J2细胞IgG吸收体外模型，通过通路阻断、蛋白免疫印迹和质谱分析等方法解析TLR2/4激活NF-κB通路和MARCHs调控FcRn表达的作用靶点和分子机制，阐明TLR2/4调控IgG吸收的具体机制。然后通过FMT技术早期干预新生仔猪，验证TLR2/4通过NF-κB通路和MARCHs调控FcRn的作用，揭示FMT提高IgG吸收中的分子机制。该研究结果不仅能深入阐明IgG转运具体调控机制，而且为功能型益生菌等调控新生仔猪先天免疫，特别是禁抗后仔猪肠道感染提供新的营养策略。

Neonatal Fc receptor FcRn-mediated milk IgG uptake dysfunction is an important cause of piglets’ low passive immunity, which causes disease or even death of piglets. However, there are few reports on the regulation mechanism of FcRn. Combining with others’ research and our previous studies, we speculated that fecal microbiota transplantation (FMT) may activate NF-κB pathway and MARCHs to regulate FcRn through TLR2/4, but its underlying molecular mechanism remains to be elucidated. In this project, firstly we use transwell plate to construct an in vitro model of IgG absorption on IPEC-J2 cell. In this model, we will explore the specific targets and molecular mechanisms of TLR2/4 mediated NF-κB pathway activation and MARCHs regulation on FcRn expression by pathway blockade, Western blot and mass spectrometry. And then to verify the mechanisms of TLR2/4 regulates FcRn and IgG, the FMT technique was used to intervene in newborn piglets. The results of this study can not only clarify the specific regulation mechanism of IgG transport, but also use it as a functional probiotic to regulate the innate immunity of newborn piglets, especially the intestinal infection of piglets after ban for antibiotics.