| Enteropathogenic Escherichia coli(enteropathogenic E.coli,EPEC)is a pathogenic bacterium that mainly infects human intestinal epithelial cells.When the bacteria infect the host,they will adhere to the surface of the epithelial cells,destroy the microvilli,and cause diarrhea.Associated with its pathogenicity,EPEC has the type III secretion system(type three secretion system,T3SS)that secretes proteins into cells.This system has a syringe-like structure.These effector proteins can help bacteria survive and reproduce.Therefore,there is a very important relationship between the infection mechanism of EPEC and the function of the effectors.The effector EspZ can inhibit host cell apoptosis and has mitochondrial localization,but its specific mechanism is not clear.In this project,24 types of effectors of the T3 SS in enteropathogenic E.coli and enterohemorrhagic E.coli were cloned.The activation or inhibition of NF-?B signaling pathway of these effectors was studied.We found that the effector EspZ can activate the NF-?B signaling pathway.We used the inhibitory activities of the effectors Nle E and Nle B on the inflammatory response to determine that the activation of the effector EspZ is similar to the TRAF6 protein.We cloned the effector protein EspZ in different A / E pathogens,and tried to find the reasons why EspZ localized on mitochondria and investigate its related biological functions by transiently expressing the effector EspZ in mammalian cells.We found that two hydrophobic sequences at the C-terminus of the effector EspZ were responsible for mitochondrial localization.The translocation expression of the effector EspZ fragmented the mitochondria of the host cells and inhibited Parkin-mediated mitochondrial autophagy.The exploration of the properties and functions of the effector EspZ provides a molecular biological basis for our research on the mechanism of the effector EspZ in inhibiting apoptosis,and helps to prevent and treat the infection of pathogenic E.coli. |
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