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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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