Two Enteropathogenic Escherichia coli Type III Secreted Proteins, EspA and EspB, Are Virulence Factors

Abe, Akio; Heczko, Ursula; Hegele, Richard G.; Brett Finlay, B.

doi:10.1084/jem.188.10.1907

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Article| November 16 1998

Two Enteropathogenic Escherichia coli Type III Secreted Proteins, EspA and EspB, Are Virulence Factors

Akio Abe,

Akio Abe

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

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Ursula Heczko,

Ursula Heczko

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

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Richard G. Hegele,

Richard G. Hegele

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

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B. Brett Finlay

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

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Author and Article Information

Akio Abe

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

Ursula Heczko

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

Richard G. Hegele

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

B. Brett Finlay

From the *Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3; the ‡Department of Bacteriology, The Kitasato Institute, Minato-ku, Tokyo 108, Japan; and the §Department of Pathology and Laboratory Medicine, St. Paul's Hospital and University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

Address correspondence to B. Brett Finlay, Biotechnology Laboratory, University of British Columbia, Rm. 237, Wesbrook Bldg., 6174 University Blvd., Vancouver, B.C., Canada V6T 1Z3. Phone: 604-822-2210; Fax: 604-822-9830; E-mail: [email protected]

A. Abe was supported by a fellowship from The Naito Foundation. U. Heczko was supported by an Erwin-Schrödinger-Fellowship (No. Jo1417-MOB) of the Fonds zur Förderung der wissenschaftlichen Forschung. This work was supported by operating grants to B.B. Finlay from the Medical Research Council of Canada and ID Vaccine Corporation, and a Howard Hughes International Research Scholar Award, and to R.G. Hegele from the Medical Research Council of Canada/British Columbia Lung Association Scholarship Award.

A. Abe and U. Heczko contributed equally to this paper.

Received: April 30 1998

Revision Received: July 21 1998

Online ISSN: 1540-9538

Print ISSN: 0022-1007

1998

J Exp Med (1998) 188 (10): 1907–1916.

https://doi.org/10.1084/jem.188.10.1907

Enteropathogenic Escherichia coli (EPEC) belongs to a family of related bacterial pathogens, including enterohemorrhagic Escherichia coli (EHEC) O157:H7 and other human and animal diarrheagenic pathogens that form attaching and effacing (A/E) lesions on host epithelial surfaces. Bacterial secreted Esp proteins and a type III secretion system are conserved among these pathogens and trigger host cell signal transduction pathways and cytoskeletal rearrangements, and mediate intimate bacterial adherence to epithelial cell surfaces in vitro. However, their role in pathogenesis is still unclear. To investigate the role of Esp proteins in disease, mutations in espA and espB were constructed in rabbit EPEC serotype O103 and infection characteristics were compared to that of the wild-type strain using histology, scanning and transmission electron microscopy, and confocal laser scanning microscopy in a weaned rabbit infection model. The virulence of EspA and EspB mutant strains was severely attenuated. Additionally, neither mutant strain formed A/E lesions, nor did either one cause cytoskeletal actin rearrangements beneath the attached bacteria in the rabbit intestine. Collectively, this study shows for the first time that the type III secreted proteins EspA and EspB are needed to form A/E lesions in vivo and are indeed virulence factors. It also confirms the role of A/E lesions in disease processes.

1998

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