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Infection and Immunity, May 2001, p. 2902-2908, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.2902-2908.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Role of Helicobacter pylori cag Region Genes in Colonization and Gastritis in Two Animal Models

Kathryn A. Eaton,1,* Dange Kersulyte,2 Megan Mefford,1 Stephen J. Danon,1,dagger Steven Krakowka,1 and Douglas E. Berg2

Department of Veterinary Biosciences, Ohio State University, Columbus, Ohio 43210,1 and Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110-10932

Received 4 December 2000/Returned for modification 19 January 2001/Accepted 7 February 2001

The Helicobacter pylori chromosomal region known as the cytotoxin-gene associated pathogenicity island (cag PAI) is associated with severe disease and encodes proteins that are believed to induce interleukin (IL-8) secretion by cultured epithelial cells. The objective of this study was to evaluate the relationship between the cag PAI, induction of IL-8, and induction of neutrophilic gastric inflammation. Germ-free neonatal piglets and conventional C57BL/6 mice were given wild-type or cag deficient mutant derivatives of H. pylori strain 26695 or SS1. Bacterial colonization was determined by plate count, gastritis and neutrophilic inflammation were quantified, and IL-8 induction in AGS cells was determined by enzyme-linked immunosorbent assay. Deletion of the entire cag region or interruption of the virB10 or virB11 homolog had no effect on bacterial colonization, gastritis, or neutrophilic inflammation. In contrast, these mutations had variable effects on IL-8 induction, depending on the H. pylori strain. In the piglet-adapated strain 26695, which induced IL-8 secretion by AGS cells, deletion of the cag PAI decreased induction. In the mouse-adapted strain SS1, which did not induce IL-8 secretion, deletion of the cagII region or interruption of any of three cag region genes increased IL-8 induction. These results indicate that in mice and piglets (i) neither the cag PAI nor the ability to induce IL-8 in vitro is essential for colonization or neutrophilic inflammation and (ii) there is no direct relationship between the presence of the cag PAI, IL-8 induction, and neutrophilic gastritis.

* Corresponding author. Mailing address: Department of Veterinary Biosciences, Ohio State University, Columbus, OH 43210. Phone: (614) 292-9667. Fax: (614) 292-6473. E-mail: eaton.1{at}osu.edu.

dagger Present address: Microbiology and Immunology, University of New South Wales, Kensington, NSW, Australia, 2033.

Infection and Immunity, May 2001, p. 2902-2908, Vol. 69, No. 5
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.5.2902-2908.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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