Avra Exerts Inhibition Of Nf-Kappa B Pathway In Its Naivesalmonellaserotype Through Suppression Of P-Jnk And Beclin-1 Molecules

Avian salmonellosis caused bySalmonella entericaserovar Enteritidis (S. Enteritidis) and Pullorum (S.Pullorum) remains a big threat to the poultry industry and public hygiene. AvrA is an effector involved in inhibiting inflammation. Compared to AvrA fromS. Enteritidis (SE-AvrA), the AvrA fromS.Pullorum (SP-AvrA) lacks ten amino acids at the C-terminal. In this study, we compared the anti-inflammatory response induced by SP-AvrA to that of SE-AvrA. Transient expression of SP-AvrA in epithelial cells resulted in significantly weaker inhibition of NF-kappa B pathway activation when treated with TNF-alpha compared to the inhibition by SE-AvrA. SP-AvrA expression in theS. Enteritidis resulted in weaker suppression of NF-kappa B pathway in infected HeLa cells compared to SE-AvrA expression in the cells, while SP-AvrA expressed inS.Pullorum C79-13 suppressed NF-kappa B activation in infected HeLa and Caco 2 BBE cells to a greater extent than did SE-AvrA because of the higher expression of SP-AvrA than SE-AvrA inS.Pullorum. Further analysis demonstrated that the inhibition of NF-kappa B pathway inSalmonella-infected cells corresponded to the downregulation of the p-JNK and Beclin-1 protein molecules. Our study reveals that AvrA modifies the anti-inflammatory response in a manner dependent on theSalmonellaserotype through inhibition of NF-kappa B pathway.