Two plasmid‐encoded genes of enteropathogenic Escherichia coli strain K798 promote invasion and survival within HEp‐2 cells. Issue 10 (22nd February 2014)

• Record Type: Journal Article
• Authors: Burska, Urszula L.; Fletcher, Jonathan N.
• Is Part Of: Apmis. Volume 122:Issue 10(2014:Oct.)
• Page Start: 922
• Page End: 930
• Publication Date: 2014-02-22
• Subjects: Pathology -- Periodicals; Microbiology -- Periodicals; Immunology -- Periodicals; 572
• DOI: 10.1111/apm.12234
• Languages: English
• ISSNs: 0903-4641

Abstract

<abstract abstract-type="main" id="apm12234-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Enteropathogenic <italic>Escherichia coli</italic> (EPEC) are considered to be extracellular pathogens, inducing attaching and effacing lesions following their attachment to the surface of eukaryotic cells; however, <italic>in vitro</italic> and <italic>in vivo</italic> invasion by EPEC has been reported in several studies. A cloned 4.6 kb fragment of EPEC plasmid pLV501 has been shown to facilitate invasion of <italic>E. coli</italic> K‐12, and here we further investigate the nature of this process. Two of the three complete open reading frames contained within the plasmid fragment have been cloned to <italic>E. coli</italic>, and in HEp‐2 adherence assays both <italic>tniA2</italic> and <italic>pecM</italic> were shown to be expressed during the first 3 h of infection from a p<italic>lac</italic> promoter. <italic>Escherichia coli</italic> transformants carrying <italic>pecM</italic> alone or in combination with <italic>tniA2</italic> were able to both survive intracellularly and escape eukaryotic cells to re‐establish themselves within the medium, whereas those bacterial cells carrying <italic>tniA2</italic> alone could not be isolated from within HEp‐2 cells after 24 h of infection, but were present in the previously sterile medium surrounding the cells. Bacteria carrying <italic>pecM</italic> and <italic>tniA2</italic> adhered to HEp‐2 cells with sites of adhesion characterized by underlying actin polymerization. The invasive potential conferred by these genes may give EPEC strains a survival advantage during prolonged infection.</p> </abstract>