ISSN:
1600-0765
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Interleukin-6 (IL-6) is thought to be a major mediator of the host's defense against infection, and it regulates immune responses in inflamed tissue. In this study, we investigated the regulation of IL-6 production in human gingival fibroblasts (HGF) and human periodontal ligament fibroblasts (HPLF). Pro-inflammatory cytokines including interleukin (IL)-lα, IL-1β and tumor necrosis factor (TNF)-α stimulated IL-6 production in HGF and HPLF in a time- and dose-dependent manner. This IL-lα, IL-lβ, or TNF-α-induced IL-6 production was enhanced, but the cAMP accumulation they induced was inhibited by the addition of indomethacin. This result suggests that endogenous prostaglandin E2 (PGE2) partially inhibits IL-l or TNF-α-induced IL-6 production, and that the enhancement of IL-6 production by IL-l or TNF-α may not be caused through endogenous PGE2-induced cAMP-dependent pathway. Dexamethasone (DEX), a glucocorticoid which is a inhibitor of nuclear factor kappa B (NF-kB) activation, markedly inhibited IL-l (α or β) or TNF-α-induced IL-6 production; so this production may be partially mediated through NF-kB. IL-l (α or β) and TNF-α enhanced IL-6 production synergistically. IL-6 production in HGF or HPLF stimulated with IL-lβ was augmented by the addition of interferon (IFN)-(gama), but was slightly suppressed by the addition of IL-4. Endogenous IL-6 enhanced IL-l (α or β)-induced IL-6 production in the presence of IL-6 soluble receptor (IL-6sR). Accordingly, in inflamed periodontal tissues, gingival fibroblasts and periodontal ligament fibroblasts stimulated with pro-inflammatory cytokines such as IL-l or TNF-α, may produce IL-6, and this production can be differentially modulated by endogenous PGE2, IL-6sR, T cell-derived cytokines such as IFN-(gama) or IL-4, and glucocorticoids.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1600-0765.1997.tb00932.x
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