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Infection and Immunity, February 2001, p. 730-736, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.730-736.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Vacuolating Cytotoxin of Helicobacter pylori Plays a Role during Colonization in a Mouse Model of Infection

Nina R. Salama,1,* Glen Otto,2 Lucy Tompkins,1 and Stanley Falkow1

Department of Microbiology and Immunology1 and Department of Comparative Medicine,2 Stanford University School of Medicine, Stanford, California 94305

Received 23 August 2000/Returned for modification 18 October 2000/Accepted 8 November 2000

Helicobacter pylori, the causative agent of gastritis and ulcer disease in humans, secretes a toxin called VacA (vacuolating cytotoxin) into culture supernatants. VacA was initially characterized and purified on the basis of its ability to induce the formation of intracellular vacuoles in tissue culture cells. H. pylori strains possessing different alleles of vacA differ in their ability to express active toxin. Those strains expressing higher toxin levels are correlated with more severe gastric disease. However, the specific role(s) played by VacA during the course of infection and disease is not clear. We have used a mouse model of H. pylori infection to begin to address this role. A null mutation of vacA compromises H. pylori in its ability to initially establish infection. If an infection by a vacA mutant is established, the bacterial load and degree of inflammation are similar to those associated with an isogenic wild-type strain. Thus, in this infection model, vacA plays a role in the initial colonization of the host, suggesting that strains of H. pylori expressing active alleles of vacA may be better adapted for host-to-host transmission.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Sherman Fairchild Science Building, D031, 299 Campus Dr., Stanford, CA 94305-5124. Phone: (650)723-2671. Fax: (650)723-1837. E-mail: nsalama{at}leland.stanford.edu

Infection and Immunity, February 2001, p. 730-736, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.730-736.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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