通过巨噬细胞自噬信号通路PI3K/AKT/mTOR来探讨大肠杆菌与机体之间的相互作用是当前研究细菌致病性的热点之一。HPI与感染过程有关，可显著增强E.coli致病性。本研究前期发现，E.coli HPI可引起单核细胞自噬关键因子LC3 mRNA的表达水平上调。为了进一步研究HPI与巨噬细胞的互作是否是通过PI3K/AKT/mTOR信号通路影响巨噬细胞自噬来提高E.coli HPI的致病性？本项目以撒坝猪源E.coli HPI为基础研究对象，运用CRISPRs-Cas9基因编辑、共聚焦显微镜、RT-PCR等现代生物学技术，探究HPI在撒坝猪源致病性E.coli感染过程中对巨噬细胞自噬信号通路PI3K/AKT/mTOR影响的分子机制，以期丰富并提升人们对E.coli HPI与巨噬细胞相互作用的认识，发现新的关键调控靶点，为如何采取有效的措施预防和控制猪大肠杆菌病提供重要理论依据。

It is one of the hotspots to study the pathogenicity of bacteria by exploring the interaction between E. coli and the body through the macrophage autophagy signal pathway PI3K/AKT/mTOR. Yersinia high pathogenicity island (HPI) is associated with the infection process and can significantly enhance the pathogenicity of E. coli. Previous studies by our group have found that E. coli HPI upregulates the expression level of autophagy key factor LC3 mRNA during infection of monocytes. To further investigate whether the interaction between HPI and macrophages improves the pathogenicity of E. coli HPI by affecting autophagy of macrophages through the PI3K/AKT/mTOR signaling pathway. This project is based on the E. coli HPI of the Saba pig, using CRISPRs-Cas9 gene editing, confocal microscopy, RT-PCR and other modern biological techniques to explore the HPI in the dam. Molecular mechanism of macrophage autophagy PI3K/AKT/mTOR signaling pathway during pathogenic E. coli infection in pigs, in order to enrich and enhance E. coli HPI and the understanding of macrophage interactions and the discovery of new key regulatory targets, and how to take effective measures to prevent and control porcine colibacillosis, provide important theoretical basis.