Soluble products from Eikenella corrodens stimulate oral epithelial cells to induce inflammatory mediators

In the inflammatory response elicited by bacterial colonization in periodontal pockets, pocket epithelial cells not only serve as a barrier to isolate the pocket microenvironment from external stimuli but also regulate the functions of neighboring cells including fibroblasts and inflammatory cells....

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Published in:Oral microbiology and immunology Vol. 16; no. 5; pp. 296 - 305
Main Authors: Yumoto, H., Nakae, H., Yamada, M., Fujinaka, K., Shinohara, C., Ebisu, S., Matsuo, T.
Format: Journal Article
Language:English
Published: Copenhagen Munksgaard International Publishers 01-10-2001
Blackwell
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Summary:In the inflammatory response elicited by bacterial colonization in periodontal pockets, pocket epithelial cells not only serve as a barrier to isolate the pocket microenvironment from external stimuli but also regulate the functions of neighboring cells including fibroblasts and inflammatory cells. To elucidate this mechanism, we characterized the effects of periodontopathic bacterium Eikenella corrodens 1073 components on the production of some inflammatory mediators in a human oral epithelial cell line (KB). In enzyme‐linked immunosorbent assay (ELISA), the E. corrodens supernatant induced interleukin‐6 (IL‐6), IL‐8 and prostaglandin E2 but not interferon‐γ (IFN‐γ) production by KB cells. After incubation with E. corrodens supernatant, KB cells showed a marked increase in the levels of IL‐6, IL‐8 and PG G/H synthase (cyclooxygenase)‐2, but not IFN‐γ, gene expression by reverse‐transcriptase polymerase chain reaction. All these E. corrodens products responsible for production of these inflammatory mediators resisted freezing and boiling and were present in a 10‐kDa filtrate. These results imply that these soluble small‐molecular‐mass products from E. corrodens stimulate various inflammatory mediator productions by human oral epithelial cells and may play a role in the initiation of periodontal inflammation and subsequently perpetuate the inflammatory response during chronic infection.
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ISSN:0902-0055
1399-302X
DOI:10.1034/j.1399-302x.2001.016005296.x