Journal Article

<i>Escherichia coli</i> and <i>Porphyromonas gingivalis</i> Lipopolysaccharide Interactions with CD14: Implications for Myeloid and Nonmyeloid Cell Activation

Mark D. Cunningham, Jürgen Bajorath, John E. Somerville and Richard P. Darveau

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 28, issue 3, pages 497-504
Published in print March 1999 | ISSN: 1058-4838
Published online March 1999 | e-ISSN: 1537-6591 | DOI: https://dx.doi.org/10.1086/515158
Escherichia coli and Porphyromonas gingivalis Lipopolysaccharide Interactions with CD14: Implications for Myeloid and Nonmyeloid Cell Activation

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Porphyromonas gingivalis, a gram-negative bacterium, is an etiologic agent for adult periodontitis. Lipopolysaccharide (LPS) released from this bacterium can react with numerous host cell types. P. gingivalis LPS stimulates tumor necrosis factor a and interleukin-1β secretion from monocytes (myeloid) but does not elicit E-selectin expression from human endothelial cells (nonmyeloid). In contrast, Escherichia coli LPS facilitates expression of these inflammatory mediators through CD14- dependent pathways on both myeloid and nonmyeloid cells. LPS binding studies have revealed that although P. gingivalis and E. coli LPSs bind to CD14 differently, this fact does not adequately explain the lack of endothelial cell activation by P. gingivalis LPS. Rather, LPS binding site and blocking monoclonal antibody epitope mapping studies have suggested that CD14 presents a charged surface that captures different microbial ligands by electrostatic interactions. We propose that human endothelial cells do not respond to P. gingivalis LPS because of their inability to “recognize” CD14-P. gingivalis LPS complexes.

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Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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