This Article Full Text (PDF) Other Versions of this Article: IAI.00519-06v1 74/11/6236    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by d'Empaire, G. Articles by Gibson, F. C. Search for Related Content PubMed PubMed Citation Articles by d'Empaire, G. Articles by Gibson, F. C., III

 Previous Article  |  Next Article 

Infect. Immun. doi:10.1128/IAI.00519-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

K1 serotype capsular polysaccharide of Porphyromonas gingivalis elicits chemokine production from murine macrophages that facilitates cell migration

Department of Oral Biology and Periodontology, Goldman School of Dental Medicine, Boston University Medical Center, Boston, MA, and Section of Infectious Diseases, Department of Medicine, Boston University Medical Center, Boston, MA, 02118.

^* To whom correspondence should be addressed. Email: frank.gibson{at}bmc.org.

	Abstract

Porphyromonas gingivalis is the principal organism associated with aggressive forms of generalized periodontal disease. Previous reports suggest that encapsulated P. gingivalis strains are more virulent then unencapsulated strains; however, the contribution of capsular polysaccharide (CPS) to the virulence of this organism is poorly understood. As periodontal disease presents with a complex inflammatory cell lesion comprised of neutrophils and monocytes, we cultured murine peritoneal macrophages with heat-killed P. gingivalis W83, CPS purified from P. gingivalis strain W83, and the 7 known serotype-specific P. gingivalis CPS and assessed the ability of supernatant fluids produced by challenged macrophages to attract naïve inflammatory cells. We also defined JE/MCP-1, KC, MIP-2, and RANTES production in response to the P. gingivalis CPS antigens. We observed that supernatant fluids collected from macrophages incubated with P. gingivalis W83 CPS and K1-serotype CPS stimulated migration of naïve murine bone marrow-derived PMNs in an in vitro cell migration chamber. W83 and K1-serotype CPS elicited potent chemokine secretion patterns from macrophages, while K2-K7 were significantly less stimulatory. RT-PCR and ELISA revealed JE/MCP-1, KC, MIP-2, and RANTES expression from murine macrophages which had been challenged with purified P. gingivalis W83 CPS. Chemokine production appeared to be dependent on both dose and time of P. gingivalis W83 CPS exposure. These data demonstrate that the P. gingivalis K1-serotype CPS elicits chemokine production from phagocytic cells. Furthermore, these data suggest that host response to this antigen may contribute to the formation of the inflammatory cell lesion observed during P. gingivalis-elicited periodontal disease.