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首页> 外文期刊>Infection and immunity >Autoregulatory Effect of Interleukin-10 on Proinflammatory Cytokine Production by Porphyromonas gingivalis Lipopolysaccharide-Tolerant Human Monocytes
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Autoregulatory Effect of Interleukin-10 on Proinflammatory Cytokine Production by Porphyromonas gingivalis Lipopolysaccharide-Tolerant Human Monocytes

机译：白介素10对牙龈卟啉单胞菌脂多糖耐人单核细胞促炎细胞因子产生的自调节作用

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Pretreatment of human peripheral blood monocytes with a very low concentration (0.1 ng/ml) of Porphyromonas gingivalislipopolysaccharides (LPS) resulted in a significant decrease of interleukin-6 (IL-6) production, but not IL-8 production, by restimulation of a high concentration (1 μg/ml) of the same LPS. In contrast, the same pretreatment with Escherichia coli LPS resulted in the enhanced production of both IL-6 and IL-8 after restimulation. The selective induction by P. gingivalis LPS tolerance of IL-6 production developed in a time-dependent manner during the primary culture. P. gingivalis LPS-pretreated cells were also refractory to a high-dose E. coli LPS restimulation in terms of IL-6 production. The expression of IL-6 mRNA decreased 10 h after restimulation of P. gingivalisLPS-pretreated monocytes. Furthermore, an up-regulation of anti-inflammatory cytokine IL-10 upon a second high-dose LPS rechallenge occurred at the same time point in the pretreated cells. We studied the role of IL-10 in the process of IL-6 down-regulation. Neutralization by an anti-IL-10 polyclonal antibody prevented IL-6 down-regulation in P. gingivalis LPS-pretreated monocytes, whereas IL-8 production was not affected. Addition of exogenous IL-10 during the high-dose LPS stimulation of untreated cells substituted for the LPS pretreatment and resulted in the inhibition of IL-6 production in a dose-dependent manner. A higher dose of IL-10 was required to suppress IL-8 synthesis from monocytes. Our data suggest that IL-10 mediates IL-6 down-regulation in P. gingivalis LPS-tolerant monocytes in an autocrine manner.
机译：极低浓度（0.1 ng / ml）牙龈卟啉单胞菌脂多糖（LPS）预处理人外周血单核细胞导致白细胞介素6（IL-6）产量显着下降，但IL却没有通过重新刺激高浓度（1μg/ ml）的相同LPS，可产生-8。相反，用大肠杆菌 LPS进行的相同预处理导致再刺激后IL-6和IL-8的产量增加。 P的选择性诱导。在初次培养过程中，牙龈对IL-6产生的LPS耐受性呈时间依赖性。 P。牙龈脂多糖预处理的细胞对高剂量的 E也是难治的。 IL-6产生对大肠杆菌LPS的再刺激。再刺激 P 10小时后，IL-6 mRNA的表达下降。牙龈 LPS预处理的单核细胞。此外，在第二次高剂量LPS​​再激发后，抗炎细胞因子IL-10的上调同时发生在预处理细胞中。我们研究了IL-10在IL-6下调过程中的作用。抗IL-10多克隆抗体的中和阻止了 P中IL-6的下调。牙龈脂多糖预处理过的单核细胞，而IL-8的产生不受影响。在高剂量LPS​​刺激未处理的细胞过程中添加外源IL-10替代了LPS预处理，并以剂量​​依赖的方式抑制了IL-6的产生。需要较高剂量的IL-10才能抑制单核细胞合成IL-8。我们的数据表明，IL-10在 P中介导IL-6下调。牙龈LPS耐受的单核细胞以自分泌方式存在。

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