The type II secretion system and its ubiquitous lipoprotein substrate, SslE, are required for biofilm formation and virulence of enteropathogenic Escherichia coli

Deborah L Baldi, Ellen E Higginson, Dianna M Hocking, Judyta Praszkier, Rosalia Cavaliere, Catherine E James, Vicki Bennett-Wood, Kristy I Azzopardi, Lynne Turnbull, Trevor J Lithgow, Roy M Robins-Browne, Cynthia B Whitchurch, Marija Tauschek

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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 either a mutation in either T2SS or SslE resulted in significantly reduced intestinal colonization and milder disease.
Original languageEnglish
Pages (from-to)2042 - 2052
Number of pages11
JournalInfection and Immunity
Volume80
Issue number6
DOIs
Publication statusPublished - 2012

Cite this

Baldi, D. L., Higginson, E. E., Hocking, D. M., Praszkier, J., Cavaliere, R., James, C. E., Bennett-Wood, V., Azzopardi, K. I., Turnbull, L., Lithgow, T. J., Robins-Browne, R. M., Whitchurch, C. B., & Tauschek, M. (2012). The type II secretion system and its ubiquitous lipoprotein substrate, SslE, are required for biofilm formation and virulence of enteropathogenic Escherichia coli. Infection and Immunity, 80(6), 2042 - 2052. https://doi.org/10.1128/IAI.06160-11