The bacterial virulence factor NleA is required for the disruption of intestinal tight junctions by enteropathogenic Escherichia coli |
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| Authors: | Ajitha Thanabalasuriar Athanasia Koutsouris rew Weflen Mark Mimee Gail Hecht Samantha Gruenheid |
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| Institution: | Department of Microbiology and Immunology, and;Complex Traits Program, The McGill Life Sciences Complex, 3649 Promenade Sir William Osler, Montreal, Quebec, H3G 0B1, Canada.;
Department of Medicine, Digestive Diseases and Nutrition, University of Illinois, Chicago, IL 60612, USA. |
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| Abstract: | 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. |
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