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Infection and Immunity, March 2001, p. 1934-1937, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1934-1937.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Human Neutrophils and Their Products Induce Shiga Toxin Production by Enterohemorrhagic Escherichia coli

Patrick L. Wagner,1 David W. K. Acheson,1 and Matthew K. Waldor1,2,*

Howard Hughes Medical Institute2 and Division of Geographic Medicine and Infectious Diseases, New England Medical Center and Tufts University School of Medicine,1 Boston, Massachusetts

Received 14 September 2000/Returned for modification 22 November 2000/Accepted 12 December 2000

The Shiga toxins (Stx) are critical virulence factors for Escherichia coli O157:H7 and other serotypes of enterohemorrhagic E. coli (EHEC). These potent toxins are encoded in the genomes of temperate lambdoid bacteriophages. We recently demonstrated that induction of the resident Stx2-encoding prophage in an O157:H7 clinical isolate is required for toxin production by this strain. Since several factors produced by human cells, including hydrogen peroxide (H2O2), are capable of inducing lambdoid prophages, we hypothesized that such molecules might also induce toxin production by EHEC. Here, we studied whether H2O2 and also human neutrophils, an important endogenous source of H2O2, induced Stx2 expression by an EHEC clinical isolate. Both H2O2 and neutrophils were found to augment Stx2 production, raising the possibility that these agents may lead to prophage induction in vivo and thereby contribute to EHEC pathogenesis.

* Corresponding author. Mailing address: Division of Geographic Medicine and Infectious Diseases, New England Medical Center #041, 750 Washington St., Boston, MA 02111. Phone: (617) 636-7618. Fax: (617) 636-5292. E-mail: mwaldor{at}lifespan.org.

Infection and Immunity, March 2001, p. 1934-1937, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1934-1937.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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