The Type II Secretion System and Its Ubiquitous Lipoprotein Substrate, SslE, Are Required for Biofilm Formation and Virulence of Enteropathogenic Escherichia coli

Author:

Baldi Deborah L.1,Higginson Ellen E.1,Hocking Dianna M.1,Praszkier Judyta1,Cavaliere Rosalia2,James Catherine E.2,Bennett-Wood Vicki1,Azzopardi Kristy I.13,Turnbull Lynne2,Lithgow Trevor4,Robins-Browne Roy M.13,Whitchurch Cynthia B.2,Tauschek Marija1

Affiliation:

1. Department of Microbiology and Immunology, The University of Melbourne, Melbourne, Australia

2. the ithree institute, University of Technology Sydney, Broadway, Australia

3. Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Australia

4. Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Australia

Abstract

ABSTRACT Enteropathogenic Escherichia coli (EPEC) is a major cause of diarrhea in infants in developing countries. We have identified a functional type II secretion system (T2SS) in EPEC that is homologous to the pathway responsible for the secretion of heat-labile enterotoxin by enterotoxigenic E. coli . The wild-type EPEC T2SS was able to secrete a heat-labile enterotoxin reporter, but an isogenic T2SS mutant could not. We showed that the major substrate of the T2SS in EPEC is SslE, an outer membrane lipoprotein (formerly known as YghJ), and that a functional T2SS is essential for biofilm formation by EPEC. T2SS and SslE mutants were arrested at the microcolony stage of biofilm formation, suggesting that the T2SS is involved in the development of mature biofilms and that SslE is a dominant effector of biofilm development. Moreover, the T2SS was required for virulence, as infection of rabbits with a rabbit-specific EPEC strain carrying a mutation in either the T2SS or SslE resulted in significantly reduced intestinal colonization and milder disease.

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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