Salmonella enteritidis Effector AvrA Stabilizes Intestinal Tight Junctions via the JNK Pathway.

ABSTRACT: Salmonella pathogenesis studies to date have focused on Salmonella typhimurium, and the pathogenesis of a second major serotype, Salmonella enteritidis, is poorly understood. Salmonella spp. possess effector proteins that display biochemical activities and modulate host functions. Here, we generated a deletion mutant of the effector AvrA, S.E-AvrA^-, and a plasmid-mediated complementary strain, S.E-AvrA^-/pAvrA⁺ (S.E-AvrA⁺), in S. Enteritidis. Using in vitro and in vivo infection models, we showed that AvrA stabilizes epithelial tight junction (TJ) proteins, such as ZO-1, in human intestinal epithelial cells. Transepithelial electrical resistance was significantly higher in cells infected with S.E-AvrA⁺ than in cells infected with S.E-Av

SUBMITTER: Lin Z 

PROVIDER: S-EPMC5207190 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature