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Infection and Immunity, June 2000, p. 3689-3695, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Role of EspB in Experimental Human Enteropathogenic Escherichia coli Infection

Carol O. Tacket,1,* Marcelo B. Sztein,1 Genevieve Losonsky,1 Akio Abe,2,dagger B. Brett Finlay,2 Barry P. McNamara,3 George T. Fantry,4 Stephen P. James,4 James P. Nataro,1 Myron M. Levine,1 and Michael S. Donnenberg4

Center for Vaccine Development1 and Divisions of Infectious Diseases3 and Gastroenterology,4 Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201, and Biotechnology Laboratory, University of British Columbia, Vancouver, British Columbia VT6 1Z3, Canada2

Received 23 December 1999/Returned for modification 28 January 2000/Accepted 10 February 2000

Enteropathogenic Escherichia coli (EPEC), a leading cause of diarrhea among infants in developing countries, induces dramatic alterations in host cell architecture that depend on a type III secretion system. EspB, one of the proteins secreted and translocated to the host cytoplasm via this system, is required for numerous alterations in host cell structure and function. To determine the role of EspB in virulence, we conducted a randomized, double-blind trial comparing the ability of wild-type EPEC and an isogenic Delta espB mutant strain to cause diarrhea in adult volunteers. Diarrhea developed in 9 of 10 volunteers who ingested the wild-type strain but in only 1 of 10 volunteers who ingested the Delta espB mutant strain. Marked destruction of the microvillous brush border adjacent to adherent organisms was observed in a jejunal biopsy from a volunteer who ingested the wild-type strain but not from two volunteers who ingested the Delta espB mutant strain. Humoral and cell-mediated immune responses to EPEC antigens were stronger among recipients of the wild-type strain. In addition, four of the volunteers who ingested the wild-type strain had lymphoproliferative responses to EspB. These results demonstrate that EspB is a critical virulence determinant of EPEC infections and suggest that EspB contributes to an immune response.

* Corresponding author. Mailing address: Center for Vaccine Development, Department of Medicine, University of Maryland School of Medicine, 685 W. Baltimore St., Baltimore, MD 21201. Phone: (410) 706-5328. Fax: (410) 706-4171. E-mail: ctacket{at}medicine.umaryland.edu.

dagger Present address: Center for Basic Research, The Kitasato Institute, Shirokane, Minato-Ku, Tokyo, Japan.

Infection and Immunity, June 2000, p. 3689-3695, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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