High pathogenicity island (HPI), which is widely distributed in Escherichia coli (E. coli), can enhance the pathogenicity of E. coli. Thus the HPI positive E. coli could pose a threat to human and animal health. It remains to be elucidated how HPI affects the virulence of pathogenic E. coli. Autophagy is an important mechanism to maintain cellular homeostasis and an innate immunity responses of organisms against pathogens. The interaction between pathogenic E. coli possessing HPI (E. coli HPI) and host autophagy system has not been reported. In this study, it was demonstrated that pathogenic E. coli induced autophagy in 3D4/21 macrophages and HPI was associated with enhanced autophagy through transmission electron microscopy, immunofluorescence and real-time PCR. The PI3K/Akt/mTOR pathway is an important negative regulatory pathway for autophagy. Through detecting the expression of key genes of PI3K/Akt/mTOR pathway, it was speculated that HPI enhanced the inhibition of the signaling pathway stimulated by pathogenic E. coli. Furthermore, HPI inhibited the secretion of IFN-γ, while the presence of HPI did not significantly affect the secretion of IL-1β. This work is the first attempt to explore the interplay between HPI carried by pathogenic E. coli and host cell autophagy. The findings might enable better understanding of the contribution of HPI to pathogenicity.

高致病性岛（HPI）在大肠杆菌（E. coli）中广泛分布，可以增强大肠杆菌的致病性。因此，HPI阳性大肠杆菌可能对人类和动物健康构成威胁。尚待阐明HPI如何影响致病性大肠杆菌的毒力。自噬是维持细胞稳态和生物体对病原体固有免疫反应的重要机制。尚未报道具有HPI的致病性大肠杆菌（E. coli HPI）与宿主自噬系统之间的相互作用。在这项研究中，证明了致病性大肠杆菌3D4 / 21巨噬细胞和HPI诱导的自噬与通过透射电子显微镜，免疫荧光和实时PCR增强的自噬有关。PI3K / Akt / mTOR途径是自噬的重要负调控途径。通过检测PI3K / Akt / mTOR途径关键基因的表达，推测HPI增强了对病原性大肠杆菌刺激的信号传导途径的抑制。此外，HPI抑制IFN-γ的分泌，而HPI的存在并未显着影响IL-1β的分泌。这项工作是探索病原性大肠杆菌携带的HPI与宿主细胞自噬之间相互作用的首次尝试。这些发现可能使人们更好地了解HPI对致病性的贡献。