The capsular polysaccharide complex of Porphyromonas gingivalis W83 and A7436 induces cytokine and chemokine production from murine peritoneal macrophages
Date
2004
DOI
Authors
D'Empaire, Gabriela
Version
OA Version
Citation
Abstract
Porphyromonas gingivalis, a Gram-negative anaerobe, is a major causative agent in the initiation and progression of severe forms of periodontal disease. The mechanism by which this gram-negative encapsulated anaerobe initiates periodontal disease is not fully known; however, bacterial and host factors are both critical to this process. Studies in a murine subcutaneous challenge model have found that encapsulated P. gingivalis caused serious forms of infection and that mice challenged with encapsulated P. gingivalis developed more severe infections than those challenged with unencapsulated strains. The precise role of P. gingivalis capsular polysaccharide in disease pathogenesis and the mechanism by which this virulence factor acts is largely unknown. In this study, we hypothese that the capsular polysaccharide of P. gingivalis promotes a cellular inflammatory response characteristic of P. gingivalis infection, and contributes to the pathology observed in chronic periodontitis. Using purified macrophages of mice, our data support that in pure form P. gingivalis CPS stimulates a potent chemokine response that is dose dependent. This data demonstrates that this antigen is a potent immunostimulatory virulence factor of P. gingivalis that may contribute to the initiation of P. gingivalis elicited periodontitis.
Description
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Thesis (M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2004 (Oral Biology).
Includes bibliographical references (leaves 63-77).
Thesis (M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2004 (Oral Biology).
Includes bibliographical references (leaves 63-77).
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.