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Infection and Immunity, March 1999, p. 1050-1055, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Role of Antibodies against Bordetella pertussis Virulence Factors in Adherence of Bordetella pertussis and Bordetella parapertussis to Human Bronchial Epithelial cells

Bernard M. van den Berg,1,* Henry Beekhuizen,1 Frits R. Mooi,2 and Ralph van Furth1

Department of Infectious Diseases, Leiden University Medical Center, Leiden,1 and Research Laboratory for Infectious Diseases, National Institute of Public Health and the Environment, Bilthoven,2 The Netherlands

Received 24 September 1998/Returned for modification 9 November 1998/Accepted 10 December 1998

Immunization with whole-cell pertussis vaccines (WCV) containing heat-killed Bordetella pertussis cells and with acellular vaccines containing genetically or chemically detoxified pertussis toxin (PT) in combination with filamentous hemagglutinin (FHA), pertactin (Prn), or fimbriae confers protection in humans and animals against B. pertussis infection. In an earlier study we demonstrated that FHA is involved in the adherence of these bacteria to human bronchial epithelial cells. In the present study we investigated whether mouse antibodies directed against B. pertussis FHA, PTg, Prn, and fimbriae, or against two other surface molecules, lipopolysaccharide (LPS) and the 40-kDa outer membrane porin protein (OMP), that are not involved in bacterial adherence, were able to block adherence of B. pertussis and B. parapertussis to human bronchial epithelial cells. All antibodies studied inhibited the adherence of B. pertussis to these epithelial cells and were equally effective in this respect. Only antibodies against LPS and 40-kDa OMP affected the adherence of B. parapertussis to epithelial cells. We conclude that antibodies which recognize surface structures on B. pertussis or on B. parapertussis can inhibit adherence of the bacteria to bronchial epithelial cells, irrespective whether these structures play a role in adherence of the bacteria to these cells.

* Corresponding author. Mailing address: Dept. of Infectious Diseases, Leiden University Medical Center, Building 1, C5-P, P.O. Box 9600, 2300 RC Leiden, The Netherlands. Phone: 31-71-5262613. Fax: 31-71-5266758. E-mail: bvdberg{at}stad.dsl.nl.

Infection and Immunity, March 1999, p. 1050-1055, Vol. 67, No. 3
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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