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Infection and Immunity, April 2002, p. 1791-1798, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1791-1798.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

In Vitro and In Vivo Characterization of a Bordetella bronchiseptica Mutant Strain with a Deep Rough Lipopolysaccharide Structure

Federico Sisti,1 Julieta Fernández,1,2 María Eugenia Rodríguez,2 Antonio Lagares,1 Nicole Guiso,3 and Daniela Flavia Hozbor1,2*

Instituto de Bioquímica y Biología Molecular,1 Centro de Investigación y Desarrollo en Fermentaciones Industriales, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, 1900 La Plata, República Argentina,2 Unité des Bordetella, Institut Pasteur, 75724 Paris Cedex 15, France3

Received 1 August 2001/ Returned for modification 1 November 2001/ Accepted 10 January 2002

Bordetella bronchiseptica is closely related to Bordetella pertussis, which produces respiratory disease primarily in mammals other than humans. However, its importance as a human pathogen is being increasingly recognized. Although a large amount of research on Bordetella has been generated regarding protein virulence factors, the participation of the surface lipopolysaccharide (LPS) during B. bronchiseptica infection is less understood. To get a better insight into this matter, we constructed and characterized the behavior of an LPS mutant with the deepest possible rough phenotype. We generated the defective mutant B. bronchiseptica LP39 on the waaC gene, which codes for a heptosyl transferase involved in the biosynthesis of the core region of the LPS molecule. Although in B. bronchiseptica LP39 the production of the principal virulence determinants adenylate cyclase-hemolysin, filamentous hemagglutinin, and pertactin persisted, the quantity of the two latter factors was diminished, with the levels of pertactin being the most greatly affected. Furthermore, the LPS of B. bronchiseptica LP39 did not react with sera obtained from mice that had been infected with the parental strain, indicating that this defective LPS is immunologically different from the wild-type LPS. In vivo experiments demonstrated that the ability to colonize the respiratory tract is reduced in the mutant, being effectively cleared from lungs within 5 days, whereas the parental strain survived at least for 30 days. In vitro experiments have demonstrated that, although B. bronchiseptica LP39 was impaired for adhesion to human epithelial cells, it is still able to survive within the host cells as efficiently as the parental strain. These results seem to indicate that the deep rough form of B. bronchiseptica LPS cannot represent a dominant phenotype at the first stage of colonization. Since isolates with deep rough LPS phenotype have already been obtained from human B. bronchiseptica chronic infections, the possibility that this phenotype arises as a consequence of selection pressure within the host at a late stage of the infection process is discussed.

* Corresponding author. Mailing address: Centro de Investigación y Desarrollo en Fermentaciones Industriales, CINDEFI, Facultad de Ciencias Exactas, Universidad Nacional de La Plata, Calles 47 y 115, 1900 La Plata, República Argentina. Phone: 54-221-483-3794. Fax: 54 221 4833794. E-mail: hozbor{at}nahuel.biol.unlp.edu.ar.

Editor: R. N. Moore

Infection and Immunity, April 2002, p. 1791-1798, Vol. 70, No. 4
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.4.1791-1798.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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