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首页> 外文期刊>Cytokine >Corticosteroids and interferons inhibit cytokine-induced production of IL-8 by human endothelial cells.
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Corticosteroids and interferons inhibit cytokine-induced production of IL-8 by human endothelial cells.

机译:皮质类固醇和干扰素抑制人血管内皮细胞因子诱导的IL-8产生。

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摘要

IL-8, secreted by endothelial cells at the site of inflammation, participates in recruitment and transmigration of leukocytes. IL-8 may also have pathophysiological consequences in inflammatory and immunological disorders. We have investigated the effect of interferons (IFNs) and glucocorticosteroids (GCs) on cytokine induced secretion and production of IL-8 by human umbilical endothelial cells (HUVEC). There was a low spontaneous secretion of IL-8 by unstimulated HUVEC which increased after 6 or 24 h of stimulation with the pro-inflammatory cytokines TNF-alpha or IL-1beta. IFN-gamma as well as the GCs, Dexamethasone and Budesonide, inhibited TNF-alpha induced IL-8 secretion in a dose-dependent manner. IFNs may have a general modulating effect, since IFN-alpha also inhibited the TNF-alpha-induced IL-8 secretion. There was a slight, but significant, increase in the content of intracellular IL-8 in stimulated HUVEC. However, there was no difference between stimulation with IL-1beta or TNF-alpha alone or in combination with IFNs or GCs, whereas inhibition of IL-8 secretion with monensin increased IL-8 content suggesting that IFNs and GCs inhibit synthesis rather than secretion of IL-8. In conclusion, IFNs or GCs may be useful for inhibiting IL-8 production by endothelial cells and could thus be used for therapeutic modulation of the inflammatory response.
机译:IL-8由炎症部位的内皮细胞分泌,参与白细胞的募集和转运。 IL-8还可能在炎症和免疫疾病中产生病理生理后果。我们已经研究了干扰素(IFNs)和糖皮质激素(GCs)对细胞因子诱导的人脐静脉内皮细胞(HUVEC)分泌和产生IL-8的影响。未刺激的HUVEC有很低的自发性IL-8分泌,在用促炎细胞因子TNF-α或IL-1beta刺激6或24小时后,IL-8分泌增加。 IFN-γ以及GC,地塞米松和布地奈德以剂量依赖的方式抑制TNF-α诱导的IL-8分泌。 IFN可能具有一般的调节作用,因为IFN-α还抑制了TNF-α诱导的IL-8分泌。在刺激的HUVEC中,细胞内IL-8的含量略有增加。然而,单独使用IL-1beta或TNF-α或与IFN或GC联合刺激之间没有差异,而莫能菌素抑制IL-8分泌会增加IL-8含量,这表明IFN和GC抑制合成而不是分泌IFN。 IL-8。总之,IFN或GC可用于抑制内皮细胞产生IL-8,因此可用于治疗性调节炎症反应。

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