IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 Baker, P. J.
Right arrow Articles by Roopenian, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Baker, P. J.
Right arrow Articles by Roopenian, D. C.

 Previous Article  |  Next Article 

Infection and Immunity, June 2000, p. 3103-3107, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Adhesion Molecule Deficiencies Increase Porphyromonas gingivalis-Induced Alveolar Bone Loss in Mice

Pamela J. Baker,1,* Lisa DuFour,2 Mark Dixon,1 and Derry C. Roopenian3

Biology Department, Bates College, Lewiston, Maine 042401; School of Dental Hygiene, University of New England, Portland, Maine 041032; and The Jackson Laboratory, Bar Harbor, Maine 046093

Received 30 September 1999/Returned for modification 29 December 1999/Accepted 1 March 2000

Alveolar bone resorption can be induced in specific-pathogen-free mice by oral infection with Porphyromonas gingivalis (P. J. Baker, R. T. Evans, and D. C. Roopenian, Arch. Oral Biol. 39:1035-1040, 1994). Here we used a mouse strain, C57BL/6J, which is relatively resistant to P. gingivalis-induced bone loss to examine whether partial or complete deletion of various adhesion molecules would increase susceptibility. Complete deletion of P-selectin or nearly complete lack of expression of intercellular adhesion molecule 1 (ICAM-1) led to increased susceptibility to bone resorption after oral infection, while a hypomorphic defect in beta 2-integrins did not. Both the total amount of bone lost and the number of sites at which there was significant loss were increased in mice deficient in either ICAM-1 or P-selectin. Each of the three adhesion molecule deficiencies was sufficient to decrease P. gingivalis-specific serum immunoglobulin G responses, but lower antibody titers did not lead to increased bone loss in partially beta 2-integrin-deficient mice. In conclusion, P-selectin and ICAM-1 deficiencies increase susceptibility to and severity of alveolar bone loss after P. gingivalis infection. This finding underscores the importance of innate immunity in protection against P. gingivalis-induced alveolar bone resorption.

* Corresponding author. Mailing address: Biology Department, Bates College, Lewiston, ME 04240. Phone: (207) 786-6108. Fax: (207) 786-8334. E-mail: pbaker{at}bates.edu.

Infection and Immunity, June 2000, p. 3103-3107, Vol. 68, No. 6
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2000 by the American Society for Microbiology. All rights reserved.