病原微生物的感染严重威胁断奶仔猪的健康，挖掘调控仔猪免疫力的营养素迫在眉睫。研究表明，TRAF6（肿瘤坏死因子受体相关因子6）是激活肠道免疫反应的关键蛋白。本课题组前期研究发现，降低m6A修饰水平能够显著抑制TRAF6的表达，而大肠杆菌感染能够显著提高TRAF6 mRNA的m6A修饰水平和效应蛋白YTHDF1的表达。为深入揭示其调控机制，本项目通过构建大肠杆菌侵染模型，在解析m6A修饰对TRAF6蛋白表达和免疫功能影响的基础上，以m6A甲基化的效应蛋白为突破口，通过免疫沉淀-质谱联用（IP-MS）蛋白组学挖掘介导效应蛋白识别TRAF6 m6A修饰的关键因子，阐明RNA m6A甲基化在肠道免疫反应中的作用及分子机制，进而从调控m6A甲基化的角度，筛选增强仔猪肠道免疫力的营养素。该研究不仅能够揭示肠道免疫应答的表观遗传学机理，也可为改善仔猪肠道免疫功能、增强仔猪抗感染能力提供新的策略。

Infection of pathogenic bacteria seriously threatens the health of weaned piglets. It is urgent to develop the nutrients regulating the immunity of piglets. TRAF6 (tumor necrosis factor receptor-related factor-6) is one of the key regulators mediating intestinal immune response, but the underlying molecular mechanism has not been elucidated. Our previous study shows that loss of m6A lead to a decreased expression of TRAF6, while Escherichia coli infection can significantly increase the level of m6A modification of TRAF6 mRNA and the expression of YTHDF1. To further reveal the mechanism, the Escherichia coli infection model is constructed. We firstly analysis of the effect of m6A modification on the expression of TRAF6 protein and immune function. Then, IP-MS (immunoprecipitation mass spectrometry) is used to identify the key factors to reveal the role and molecular mechanism of RNA m6A methylation in intestinal immunity to defense against Escherichia coli infection. Finally, we screen the nutrients to enhance the intestinal immunity of piglets by m6A methylation. This study will not only reveal the epigenetic mechanism of intestinal immune response, but also provide new ideas for improving the intestinal immune function of piglets.