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Infection and Immunity, November 1999, p. 5972-5978, Vol. 67, No. 11
Department of Veterinary Pathology,
University of Glasgow Veterinary School, Garscube Estate, Glasgow G61
1QH, Scotland,1 and Vaccine Research
Unit, Department of Biochemistry, Imperial College of Science,
Technology and Medicine, London SW7 2AZ,
England2
Received 12 April 1999/Returned for modification 26 May
1999/Accepted 30 August 1999
The effect of Bordetella bronchiseptica infection on
the viability of murine macrophage-like cells and on primary porcine alveolar macrophages was investigated. The bacterium was shown to be
cytotoxic for both cell types, particularly where tight cell-to-cell
contacts were established. In addition, bvg mutants were
poorly cytotoxic for the eukaryotic cells, while a prn
mutant was significantly less toxic than wild-type bacteria. B. bronchiseptica-mediated cytotoxicity was inhibited in the
presence of cytochalasin D or cycloheximide, an inhibitor of
microfilament-dependent phagocytosis or de novo eukaryotic protein
synthesis, respectively. The mechanism of eukaryotic cell death was
examined, and cell death was found to occur primarily through a
necrotic pathway, although a small proportion of the population
underwent apoptosis.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Bordetella bronchiseptica-Mediated
Cytotoxicity to Macrophages Is Dependent on bvg-Regulated
Factors, Including Pertactin

*
Corresponding author. Mailing address: Department of
Veterinary Pathology, University of Glasgow Veterinary School, Garscube Estate, Bearsden Rd., Glasgow G61 1QH, Scotland. Phone: 141 330 5780. Fax: 141 330 5602. E-mail:
m.roberts{at}vet.gla.ac.uk.
Present address: Department of Immunology, St. Bartholomew's and
The Royal London School of Medicine and Dentistry, London EC1A 7BE, England.
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