Escherichia coli O157:H7 suppresses host autophagy and promotes epithelial adhesion via Tir-mediated and cAMP-independent activation of protein kinase A.

ABSTRACT: Autophagy is a pivotal innate immune response that not only degrades cytosolic components, but also serves as one of the critical antimicrobial mechanisms eliminating intracellular pathogens. However, its role in host defense against extracellular pathogens is largely unknown. Here we showed that E. coli O157:H7 altered autophagy to evade host defense and facilitate adhesion. Enhancing host cell autophagy with tumor necrosis factor (TNF), host starvation or rapamycin reduced the adherence of E. coli O157:H7 to HT-29 cells. As a key regulator of autophagy, protein kinase A (PKA) was activated by E. coli O157:H7 infection. PKA inhibition by H89 abrogated E. coli O157:H7 inhibition of autophagy and prevented bacterial epithelial adhesion. Thus, PKA had a mediatory

SUBMITTER: Xue Y 

PROVIDER: S-EPMC5624281 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature