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 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Copenhagen
Munksgaard International Publishers
01-10-2001
Blackwell |
Subjects: | |
Online Access: | Get full text |
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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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Bibliography: | ArticleID:OMI160507 istex:AFD70475E5610D1DDCBE9AFEFC2CE69FE5CD9E63 ark:/67375/WNG-ZXQK8LT1-B ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0902-0055 1399-302X |
DOI: | 10.1034/j.1399-302x.2001.016005296.x |