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首页> 外文期刊>Infection and immunity >Human Gingival CD14+ Fibroblasts Primed with Gamma Interferon Increase Production of Interleukin-8 in Response to Lipopolysaccharide through Up-Regulation of Membrane CD14 and MyD88 mRNA Expression
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Human Gingival CD14+ Fibroblasts Primed with Gamma Interferon Increase Production of Interleukin-8 in Response to Lipopolysaccharide through Up-Regulation of Membrane CD14 and MyD88 mRNA Expression

机译：γ干扰素引发的人牙龈CD14 +成纤维细胞通过膜CD14和MyD88 mRNA表达的上调增加了对脂多糖的应答，使白介素8的产生增加。

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Gamma interferon (IFN-γ)-primed human gingival fibroblasts (HGF) have been shown to produce higher levels of interleukin-8 (IL-8) upon stimulation with bacterial products and inflammatory cytokines than nonprimed controls. In this study, we examined whether priming of HGF with IFN-γ up-regulates IL-8 production by the cells in response to purified lipopolysaccharide (LPS). The priming effect of IFN-γ was clearly observed in the high-CD14-expressing (CD14high) HGF but not in the low-CD14-expressing (CD14low) HGF. The CD14high HGF were most effectively primed with IFN-γ (1,000 IU/ml) for 72 h. To elucidate the mechanism of the priming effects of IFN-γ for the LPS response by HGF, we examined whether IFN-γ regulated expression of CD14, Toll-like receptor 2 (TLR2), TLR4, MD-2, and MyD88, all of which are molecules suggested to be associated with LPS signaling. In CD14high HGF, IFN-γ markedly up-regulated CD14 and MyD88 but not TLR4 protein and MD-2 mRNA expression, while in CD14low HGF, IFN-γ slightly increased MyD88 and scarcely affected CD14, TLR4 protein, and MD-2 mRNA levels. LPS-induced IL-8 production by IFN-γ-primed CD14high HGF was significantly inhibited by monoclonal antibodies (MAbs) against CD14 and TLR4, but not by an anti-TLR2 MAb. These findings suggested that IFN-γ primed CD14high HGF to enhance production of IL-8 in response to LPS through augmentation of the CD14-TLR system, where the presence of membrane CD14 was indispensable for the response of HGF to LPS.
机译：γ干扰素（IFN-γ）引发的人牙龈成纤维细胞（HGF）已显示在细菌产品和炎性细胞因子刺激下产生的白细胞介素8（IL-8）水平高于未引发对照的白细胞介素8（IL-8）。在这项研究中，我们检查了用IFN-γ引发HGF是否能上调细胞响应纯化的脂多糖（LPS）产生IL-8。在高表达CD14（CD14 high ）的HGF中明显观察到了IFN-γ的启动作用，而在低CD14表达（CD14 low ）的HGF中却没有观察到。 CD14 sup HGF最有效地用IFN-γ（1,000 IU / ml）灌注72 h。为了阐明IFN-γ引发HGF对LPS应答的作用机制，我们检查了IFN-γ是否调节CD14，Toll样受体2（TLR2），TLR4，MD-2和MyD88的表达，所有它们是与LPS信号传导相关的分子。在CD14 high HGF中，IFN-γ明显上调CD14和MyD88，但不显着上调TLR4蛋白和MD-2 mRNA的表达，而在CD14 low HGF中，IFN-γ轻微上调增加MyD88，几乎不影响CD14，TLR4蛋白和MD-2 mRNA水平。抗CD14和TLR4的单克隆抗体（MAb）显着抑制IFN-γ引发的CD14 sup> HGF对LPS诱导的IL-8的产生，但抗TLR2 MAb则没有抑制作用。这些发现表明，IFN-γ引发的CD14 high HGF通过增强CD14-TLR系统来增强对LPS的IL-8产生，而CD14-TLR系统的存在是不可缺少的。 HGF转换为LPS。

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