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首页> 外文期刊>Cytokine >Inhibited proliferation of human lung fibroblasts by LPS is through IL-6 and IL-8 release.
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Inhibited proliferation of human lung fibroblasts by LPS is through IL-6 and IL-8 release.

机译:LPS抑制人肺成纤维细胞的增殖是通过IL-6和IL-8的释放。

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Through the consideration of decreased proliferation of lung fibroblasts from subjects with chronic obstructive pulmonary disease (COPD) and the proinflammatory role of lipopolysaccharide (LPS) in the COPD development, we hypothesized that LPS might inhibit proliferation in lung fibroblasts and the possible mechanism was investigated. Primary human lung fibroblasts were cultured from peripheral lung tissue and then treated with or without LPS. Proliferation was measured by AlamarBlue(R) assay. Levels of TNF-alpha, IL-6, IL-8, IL-12p70, IL-1beta and IL-10 in the supernatants were measured by ELISA. The mRNA of histone deacetylases 2 (HDAC2) was analyzed using real-time PCR. LPS appeared to have a dose-dependent inhibitory effect on fibroblasts proliferation. The concentrations of IL-6 and IL-8 in the treatment culture media were significantly increased, accompanied by a reduced mRNA expression of HDAC2. IL-6 or IL-8 itself led to the reduction of fibroblasts proliferation. Treatment with 1 ng/ml TNF-alpha in fibroblasts also caused a significant decrease in proliferation and an increase in the production of IL-8 and IL-6. Our data suggest that LPS can inhibit the proliferation of in vitro human lung fibroblasts at least through a production of IL-6 and IL-8. The cytokine response is related to the decreased HDAC2 transcription.
机译:通过考虑慢性阻塞性肺疾病(COPD)受试者肺成纤维细胞增殖减少以及脂多糖(LPS)在COPD发育中的促炎作用,我们假设LPS可能抑制肺成纤维细胞增殖并研究了可能的机制。从周围肺组织培养原代人肺成纤维细胞,然后用或不用LPS进行处理。通过AlamarBlue测定来测量增殖。通过ELISA测量上清液中TNF-α,IL-6,IL-8,IL-12p70,IL-1β和IL-10的水平。组蛋白脱乙酰基酶2(HDAC2)的mRNA使用实时PCR分析。 LPS对成纤维细胞的增殖似乎具有剂量依赖性的抑制作用。治疗培养基中IL-6和IL-8的浓度显着增加,同时HDAC2的mRNA表达降低。 IL-6或IL-8本身导致成纤维细胞增殖减少。在成纤维细胞中用1 ng / mlTNF-α进行治疗也引起增殖的显着下降和IL-8和IL-6产量的增加。我们的数据表明,LPS至少可以通过产生IL-6和IL-8抑制体外人肺成纤维细胞的增殖。细胞因子反应与减少的HDAC2转录有关。

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