Open AccessThe bacterial virulence factor NleA is required for the disruption of intestinal tight junctions by enteropathogenic Escherichia coli
Author(s) -
Thanabalasuriar Ajitha,
Koutsouris Athanasia,
Weflen Andrew,
Mimee Mark,
Hecht Gail,
Gruenheid Samantha
Publication year - 2010
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2009.01376.x
Subject(s) - enteropathogenic escherichia coli , biology , effector , virulence , secretion , type three secretion system , tight junction , microbiology and biotechnology , barrier function , gene , genetics , biochemistry
Summary Enteropathogenic Escherichia coli (EPEC) is a diarrhoeal pathogen that adheres to epithelial cells of the small intestine and uses a type III secretion system to inject effector proteins into host cells. EPEC infection leads to disruption of host intestinal tight junctions that are important for maintaining intestinal barrier function. This disruption is dependent on the bacterial type III secretion system, as well as the translocated effectors EspF and Map. Here we show that a third type III translocated bacterial effector protein, NleA, is also involved in tight junction disruption during EPEC infection. Using the drug Brefeldin A, we demonstrate that the effect of NleA on tight junction integrity is related to its inhibition of host cell protein trafficking through COPII‐dependent pathways. These results suggest that NleA's striking effect on virulence is mediated, at least in part, via its role in disruption of intestinal barrier function.