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Infection and Immunity, June 2004, p. 3252-3259, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3252-3259.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Therapeutic Vaccination against Helicobacter pylori in the Beagle Dog Experimental Model: Safety, Immunogenicity, and Efficacy

Giacomo Rossi,1,{dagger} Paolo Ruggiero,2*,{dagger} Samuele Peppoloni,2,{ddagger} Laura Pancotto,2 Damiano Fortuna,3 Laura Lauretti,2 Gianfranco Volpini,2 Silvia Mancianti,2 Michele Corazza,3 Ennio Taccini,4 Francesco Di Pisa,5 Rino Rappuoli,2 and Giuseppe Del Giudice2

Department of Veterinary Science, University of Camerino, Camerino,1 IRIS Research Center,2 Technology Development, Chiron s.r.l., Siena,5 Departments of Veterinary Clinic,3 Animal Pathology, University of Pisa, Pisa, Italy4

Received 5 September 2003/ Returned for modification 9 January 2004/ Accepted 5 March 2004

Helicobacter pylori is a gram-negative bacterium that colonizes the human gastric mucosa causing gastritis and peptic ulcer and increasing the risk of gastric cancer. The efficacy of current antibiotic-based therapies can be limited by problems of patient compliance and increasing antibiotic resistance; the vaccine approach can overcome these limits. The present study describes the therapeutic vaccination of experimentally H. pylori-infected beagle dogs, an animal model that reproduces several aspects of the human infection with H. pylori. The vaccine consisted of three recombinant H. pylori antigens, CagA, VacA, and NAP, formulated at different doses (10, 25, or 50 µg each) with alum and administered intramuscularly either weekly or monthly. No adverse effects were observed after vaccination and a good immunoglobulin G response was generated against each of the three antigens. Bacterial colonization and gastritis were decreased after the completion of the vaccination cycle, especially in the case of the monthly immunization schedule. In conclusion, therapeutic vaccination in the beagle dog model was safe and immunogenic and was able to limit H. pylori colonization and the related gastric pathology.

* Corresponding author. Mailing address: IRIS Research Center, Chiron s.r.l., Via Fiorentina 1, I-53100 Siena, Italy. Phone: 39-0577-243111. Fax: 39-0577-243564. E-mail: paolo_ruggiero{at}chiron.it.

Editor: A. D. O'Brien

{dagger} G.R. and P.R. contributed equally to this study.

{ddagger} Present address: Department of Hygiene, Microbiology and Biostatistics, University of Modena and Reggio Emilia, Modena, Italy.

Infection and Immunity, June 2004, p. 3252-3259, Vol. 72, No. 6
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.6.3252-3259.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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