通过细胞焦亡信号通路来探讨宿主与微生物之间的相互作用是当前研究细菌致病性的新前沿。HPI是E.coli的主要毒力因子之一，可显著增强E.coli摄铁能力，提高其致病性。本课题组以往的研究表明，HPI可通过摄取铁降低PMN细胞内的ROS水平，抑制其呼吸爆发，进而提高E.coli的致病性。为了进一步研究HPI是否通能过NRLP3/ASC/Caspase-1信号通路影响小肠上皮细胞焦亡来提高E.coli的致病性？本项目以云南撒坝猪E.coli为研究对象，运用CRISPRs-Cas9基因编辑、共聚焦显微镜、荧光定量PCR、western blot、免疫组化等现代生物学技术，研究HPI在撒坝猪E.coli感染过程中对小肠上皮细胞NRLP3/ASC/Caspase-1信号通路的影响，并阐明其作用的机制，以期丰富并提升人们对E.coli与肠道上皮细胞相互作用的认识，为该病的防制提供新思路。

Pyroptosis signaling pathway is a new frontier for exploring the interaction between host and microbial. HPI is one of the main virulence factors of E.coli, which can significantly enhance the capacity of iron taken in and improve the pathogenicity of E. coli. Our previous studies have indicated that HPI can inhibit the breathing outbreak of PMN by lowering the levels of intracellular ROS through iron intake in. Whether the HPI can improve the pathogenic ability of E. coli through NRLP3/ASC/Caspase-1 pyroptosis signaling pathway on intestinal epithelial cells need ferther study. In this research, the NRLP3/ASC/Caspase-1 signaling pathway of intestinal epithelial cell will be test by CRISPRs-Cas9,Real-time PCR, confocal microscopy,immunocytochemistry,protein imprinting technology et al. The results are very important scientific significance for enriching and promoting the cognitive level of the interaction between pathogenic E. coli and intestinal epithelium, which can provide novel approaches to prevent and control of colibacillosis.