Interleukin-1β Modulates Proinflammatory Cytokine Production in Human Epithelial Cells
Proinflammatory cytokine
Interleukin 8
DOI:
10.1128/iai.01428-07
Publication Date:
2008-03-11T01:05:47Z
AUTHORS (8)
ABSTRACT
ABSTRACT Periodontitis is a chronic human inflammatory disease initiated and sustained by dental plaque microorganisms. A major contributing pathogen Porphyromonas gingivalis , gram-negative bacterium recognized Toll-like receptor 2 (TLR2) TLR4, which are expressed gingival epithelial cells (HGECs). However, it still unclear how these respond to P. initiate immune responses. We have reported previously that HGECs produce wide range of proinflammatory cytokines, including interleukin-6 (IL-6), IL-8, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor alpha (TNF-α), IL-1β. In this study, we show IL-1β has special role in the modulation other cytokines challenged with . Our results increased production correlates cell surface expression more specifically, TLR4-normal fourfold than do TLR4-deficient after challenge. Moreover, blocking greatly reduces “secondary” such as IL-8 or IL-6. data indicate induction plays an important mediating release from primary following challenge process may be enhancement mechanism adopted cells.
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