This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Alonso, S.
Right arrow Articles by Locht, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Alonso, S.
Right arrow Articles by Locht, C.

 Previous Article  |  Next Article 

Infection and Immunity, October 2001, p. 6038-6043, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6038-6043.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Role of ADP-Ribosyltransferase Activity of Pertussis Toxin in Toxin-Adhesin Redundancy with Filamentous Hemagglutinin during Bordetella pertussis Infection

Sylvie Alonso, Kévin Pethe, Nathalie Mielcarek, Dominique Raze, and Camille Locht*

INSERM U447, IBL, Institut Pasteur de Lille, F-59019 Lille, France

Received 5 June 2001/Returned for modification 10 July 2001/Accepted 18 July 2001

Pertussis toxin (PT) and filamentous hemagglutinin (FHA) are two major virulence factors of Bordetella pertussis. FHA is the main adhesin, whereas PT is a toxin with an A-B structure, in which the A protomer expresses ADP-ribosyltransferase activity and the B moiety is responsible for binding to the target cells. Here, we show redundancy of FHA and PT during infection. Whereas PT-deficient and FHA-deficient mutants colonized the mouse respiratory tract nearly as efficiently as did the isogenic parent strain, a mutant deficient for both factors colonized substantially less well. This was not due to redundant functions of PT and FHA as adhesins, since in vitro studies of epithelial cells and macrophages indicated that FHA, but not PT, acts as an adhesin. An FHA-deficient B. pertussis strain producing enzymatically inactive PT colonized as poorly as did the FHA-deficient, PT-deficient strain, indicating that the ADP-ribosyltransferase activity of PT is required for redundancy with FHA. Only strains producing active PT induced a local transient release of tumor necrosis factor alpha (TNF-alpha ), suggesting that the pharmacological effects of PT are the basis of the redundancy with FHA, through the release of TNF-alpha . This may lead to damage of the pulmonary epithelium, allowing the bacteria to colonize even in the absence of FHA.

* Corresponding author. Mailing address: INSERM U447, IBL, Institut Pasteur de Lille, 1, rue du Pr. Calmette, F-59019 Lille, France. Phone: (33) 3 20 87 11 51. Fax: (33) 3 20 87 11 58. E-mail: camille.locht{at}pasteur-lille.fr.

Infection and Immunity, October 2001, p. 6038-6043, Vol. 69, No. 10
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.10.6038-6043.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Ho, S. Y., Chua, S. Q., Foo, D. G. W., Locht, C., Chow, V. T., Poh, C. L., Alonso, S. (2008). Highly Attenuated Bordetella pertussis Strain BPZE1 as a Potential Live Vehicle for Delivery of Heterologous Vaccine Candidates. Infect. Immun. 76: 111-119 [Abstract] [Full Text]  
  • Inatsuka, C. S., Julio, S. M., Cotter, P. A. (2005). Bordetella filamentous hemagglutinin plays a critical role in immunomodulation, suggesting a mechanism for host specificity. Proc. Natl. Acad. Sci. USA 102: 18578-18583 [Abstract] [Full Text]  
  • Alonso, S., Willery, E., Renauld-Mongenie, G., Locht, C. (2005). Production of Nontypeable Haemophilus influenzae HtrA by Recombinant Bordetella pertussis with the Use of Filamentous Hemagglutinin as a Carrier. Infect. Immun. 73: 4295-4301 [Abstract] [Full Text]  
  • Carbonetti, N. H., Artamonova, G. V., Andreasen, C., Dudley, E., Mays, R. M., Worthington, Z. E. V. (2004). Suppression of Serum Antibody Responses by Pertussis Toxin after Respiratory Tract Colonization by Bordetella pertussis and Identification of an Immunodominant Lipoprotein. Infect. Immun. 72: 3350-3358 [Abstract] [Full Text]  
  • Carbonetti, N. H., Artamonova, G. V., Mays, R. M., Worthington, Z. E. V. (2003). Pertussis Toxin Plays an Early Role in Respiratory Tract Colonization by Bordetella pertussis. Infect. Immun. 71: 6358-6366 [Abstract] [Full Text]  
  • Coutte, L., Alonso, S., Reveneau, N., Willery, E., Quatannens, B., Locht, C., Jacob-Dubuisson, F. (2003). Role of Adhesin Release for Mucosal Colonization by a Bacterial Pathogen. JEM 197: 735-742 [Abstract] [Full Text]  
  • Antoine, R., Jacob-Dubuisson, F., Drobecq, H., Willery, E., Lesjean, S., Locht, C. (2003). Overrepresentation of a Gene Family Encoding Extracytoplasmic Solute Receptors in Bordetella. J. Bacteriol. 185: 1470-1474 [Abstract] [Full Text]  
  • Alonso, S., Reveneau, N., Pethe, K., Locht, C. (2002). Eighty-Kilodalton N-Terminal Moiety of Bordetella pertussis Filamentous Hemagglutinin: Adherence, Immunogenicity, and Protective Role. Infect. Immun. 70: 4142-4147 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»