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首页> 外文期刊>Cytokine >Cardiotrophin-1 induces interleukin-6 synthesis in human monocytes.
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Cardiotrophin-1 induces interleukin-6 synthesis in human monocytes.

机译：心肌营养素1诱导人单核细胞中白介素6的合成。

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BACKGROUND: Patients with congestive heart failure (CHF) show increased serum concentrations of cytokines like interleukin-6 (IL-6) and cardiotrophin-1 (CT-1). Additionally, monocyte function is modulated in CHF. The aim of this study was to examine if CT-1 is able to induce IL-6 in human monocytes and to investigate the underlying pathway. METHODS: Separated peripheral blood monocytes of healthy volunteers were cultured with increasing concentrations of CT-1 for different periods. IL-6 mRNA was determined by RT-PCR or real-time PCR and IL-6 protein concentration in the supernatant by ELISA. Phosphorylation of signal transducer and activation of transcription (STAT) 3 was analyzed by western blot or by FACS analysis. To clarify the signalling pathway of CT-1 induced IL-6 expression various inhibitors of possible signal transducing molecules were used. RESULTS: CT-1 induced IL-6 mRNA in monocytes in a time- and concentration-dependent manner. Maximal mRNA induction was detectable after 6h with 100 ng/mlCT-1. IL-6 protein also increased in a time- and concentration-dependent manner with a maximum after 48 h with 100 ng/ml CT-1. AG490 as well as SB 203580 and parthenolide blocked CT-1 induced IL-6 expression completely. AG 490 was able to inhibit STAT3 phosphorylation in western blot analysis completely. This indicates that JAK2/STAT3, p38 and nuclear factor kappaB (NFkappaB) are involved in this pathway. To exclude a possible influence of plastic adherence of monocytes on CT-1 induced IL-6 expression, we determined intracellular STAT3 phosphorylation in whole blood samples by FACS analysis and observed independently of culture conditions a CT-1 concentration-dependent STAT3 phosphorylation. CONCLUSION: CT-1 induces IL-6 mRNA and protein expression in a time- and concentration-dependent manner. The underlying pathway is Janus kinase (JAK)2/STAT3, p38 and NFkappaB dependent. These data may explain increased IL-6 serum concentrations and altered monocyte function found in patients with CHF. Modulation of the CT-1 pathway might be a interesting strategy in the treatment of CHF.
机译：背景：患有充血性心力衰竭（CHF）的患者血清中的白细胞介素6（IL-6）和心肌营养素1（CT-1）等细胞因子浓度升高。另外，单核细胞功能在CHF中被调节。这项研究的目的是检查CT-1是否能够在人单核细胞中诱导IL-6并研究其潜在途径。方法：分离健康志愿者的外周血单核细胞，并在不同时期内增加其CT-1的浓度。通过RT-PCR或实时PCR测定IL-6 mRNA，并通过ELISA测定上清液中IL-6蛋白浓度。信号转导的磷酸化和转录激活（STAT）3通过蛋白质印迹或流式细胞仪分析进行了分析。为了阐明CT-1诱导的IL-6表达的信号传导途径，使用了各种可能的信号传导分子抑制剂。结果：CT-1以时间和浓度依赖性方式诱导单核细胞中IL-6 mRNA的表达。用100 ng / mlCT-1检测6小时后可检测到最大的mRNA诱导。 IL-6蛋白也以时间和浓度依赖性的方式增加，在使用100 ng / ml CT-1的48小时后达到最大值。 AG490以及SB 203580和小白菊内酯完全阻断了CT-1诱导的IL-6表达。在蛋白质印迹分析中，AG 490能够完全抑制STAT3磷酸化。这表明JAK2 / STAT3，p38和核因子κB（NFkappaB）参与了该途径。为了排除单核细胞塑料粘附对CT-1诱导的IL-6表达的可能影响，我们通过FACS分析确定了全血样品中的细胞内STAT3磷酸化，并且独立于培养条件观察到了CT-1浓度依赖性STAT3磷酸化。结论：CT-1以时间和浓度依赖性方式诱导IL-6 mRNA和蛋白表达。潜在的途径是Janus激酶（JAK）2 / STAT3，p38和NFkappaB依赖性。这些数据可能解释了CHF患者发现的IL-6血清浓度升高和单核细胞功能改变。 CT-1途径的调节可能是治疗CHF的有趣策略。

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