Host autophagy and inflammasome in E. coli O157:H7 intestinal colonization

发布时间: 2017-07-04 来源:

  报告题目:Host autophagy and inflammasome in E. coli O157:H7 intestinal colonization

  报告人:ZHU MEIJUN Associate Professor, School of Food Science, Washington State University

  报告时间:2017.7.5 (星期三) 上午10:00


  邀请人:马旅雁 研究员


  Escherichia coli O157:H7 is an important foodborne pathogen that causes serious illness in

  humans at low infectious doses. E. coli O157:H7 produces Shiga toxins that cause hemorrhagic colitis, hemolytic uremic syndrome and acute renal failure in humans. In addition, it can intimately attach to the intestinal epithelial cells causing attaching and effacing lesion. E. coli O157:H7 interaction with gut tissues depends on its ability to adhere to the host cells. 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. We recently showed that E. coli O157:H7 alters autophagy to evade host defense, which favors bacterial persistence on epithelial cell surfaces and facilitates adhesion; translocated intimin receptor (Tir) and protein kinase A (PKA) plays a pivotal role in manipulating host autophagy during infection. Parallelly, E. coli O157:H7 infection induces LRR and PYD domains-containing protein 3 (NLRP3) inflammasome assembly and activation, resulting in mitochondrial dysfunction and production of reactive oxygen species (ROS). Quercetin, one of the most important flavonoids in plant origin foods, has a protective role in inhibiting NLRP3 activation upon E. coli O157:H7 infection and augments autophagy activation, exerting preventive roles in host cells upon E. coli O157:H7 infection.