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Infection and Immunity, June 1999, p. 3112-3120, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

A Conventional Beagle Dog Model for Acute and Chronic Infection with Helicobacter pylori

Giacomo Rossi,1 Michela Rossi,2 Claudia G. Vitali,1 Damiano Fortuna,1 Daniela Burroni,2 Laura Pancotto,2 Sonia Capecchi,2 Sabrina Sozzi,1 Giacomo Renzoni,1 Giovanni Braca,1 Giuseppe Del Giudice,2 Rino Rappuoli,2,* Paolo Ghiara,2 and Ennio Taccini1

Department of Animal Pathology, Prophylaxis and Food Hygiene, University of Pisa, 50100 Pisa,1 and IRIS, Chiron SpA Immunobiological Research Institute Siena, 53100 Siena,2 Italy

Received 18 November 1998/Returned for modification 4 February 1999/Accepted 1 March 1999

Helicobacter pylori has been widely recognized as an important human pathogen responsible for chronic gastritis, peptic ulcers, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma. Little is known about the natural history of this infection since patients are usually recognized as having the infection only after years or decades of chronic disease. Several animal models of H. pylori infection, including those with different species of rodents, nonhuman primates, and germ-free animals, have been developed. Here we describe a new animal model in which the clinical, pathological, microbiological, and immunological aspects of human acute and chronic infection are mimicked and which allows us to monitor these aspects of infection within the same individuals. Conventional Beagle dogs were infected orally with a mouse-adapted strain of H. pylori and monitored for up to 24 weeks. Acute infection caused vomiting and diarrhea. The acute phase was followed by polymorphonuclear cell infiltration, interleukin 8 induction, mononuclear cell recruitment, and the appearance of a specific antibody response against H. pylori. The chronic phase was characterized by gastritis, epithelial alterations, superficial erosions, and the appearance of the typical macroscopic follicles that in humans are considered possible precursors of MALT lymphoma. In conclusion, infection in this model mimics closely human infection and allows us to study those phases that cannot be studied in humans. This new model can be a unique tool for learning more about the disease and for developing strategies for treatment and prevention.

* Corresponding author. Mailing address: Chiron SpA Immunobiological Research Institute Siena, Via Fiorentina 1, 53100 Siena, Italy. Phone: 39-0577-243414. Fax: 39-0577-243564. E-mail: rappuoli{at}iris02.biocine.it.

Infection and Immunity, June 1999, p. 3112-3120, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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