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Infection and Immunity, April 2009, p. 1304-1314, Vol. 77, No. 4
0019-9567/09/$08.00+0     doi:10.1128/IAI.01351-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Modelling of Infection by Enteropathogenic Escherichia coli Strains in Lineages 2 and 4 Ex Vivo and In Vivo by Using Citrobacter rodentium Expressing TccP{triangledown}

Francis Girard,{dagger} Valérie F. Crepin,{dagger} and Gad Frankel*

Centre for Molecular Microbiology and Infection, Division of Cell and Molecular Biology, Imperial College London, SW7 2AZ London, United Kingdom

Received 5 November 2008/ Returned for modification 31 December 2008/ Accepted 28 January 2009

Enteropathogenic Escherichia coli (EPEC) strains colonize the human gut mucosa via attaching-and-effacing (A/E) lesion formation, while in vitro they employ diverse strategies to trigger actin polymerization. Strains belonging to the EPEC-1 lineage trigger strong actin polymerization via tyrosine phosphorylation of the type III secretion system (T3SS) effector Tir, recruitment of Nck, and activation of N-WASP. Strains belonging to EPEC-2 and EPEC-4 can trigger strong actin polymerization by dual mechanisms, since while employing the Tir-Nck pathway they can additionally activate N-WASP via the T3SS effectors TccP2 and TccP, respectively. It is currently not known if the ability to trigger actin polymerization by twin mechanisms increases in vivo virulence or fitness. Since mice are resistant to EPEC infection, in vivo studies are frequently done using the murine model pathogen Citrobacter rodentium, which shares with EPEC-1 strains the ability to induce A/E lesions and trigger strong actin polymerization via the Tir:Nck pathway. In order to model infections with EPEC-2 and EPEC-4, we constructed C. rodentium strains expressing TccP. Using a mouse intestinal in vitro organ culture model and oral gavage into C57BL/6 mice, we have shown that TccP can cooperate with Tir of C. rodentium. The recombinant strains induced typical A/E lesions ex vivo and in vivo. Expression of TccP did not alter C. rodentium colonization dynamics or pathology. In competition with the wild-type strain, expression of TccP in C. rodentium did not confer a competitive advantage.

* Corresponding author. Mailing address: CMMI, Flowers Building, Imperial College London, London SW7 2AZ, United Kingdom. Phone: 44 020 2594 5253. Fax: 44 020 5794 3069. E-mail: g.frankel{at}imperial.ac.uk

{triangledown} Published ahead of print on 2 February 2009.

Editor: A. J. Bäumler

{dagger} These two authors contributed equally to this work.

Infection and Immunity, April 2009, p. 1304-1314, Vol. 77, No. 4
0019-9567/09/$08.00+0     doi:10.1128/IAI.01351-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Girard, F., Dziva, F., Stevens, M. P., Frankel, G. (2009). Interactions of Typical and Atypical Enteropathogenic Escherichia coli Strains with the Calf Intestinal Mucosa Ex Vivo. Appl. Environ. Microbiol. 75: 5991-5995 [Abstract] [Full Text]  


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