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首页> 外文期刊>Cytokine >Post-transcriptional silencing of CCR3 downregulates IL-4 stimulated release of eotaxin-3 (CCL26) and other CCR3 ligands in alveolar type II cells.
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Post-transcriptional silencing of CCR3 downregulates IL-4 stimulated release of eotaxin-3 (CCL26) and other CCR3 ligands in alveolar type II cells.

机译：CCR3的转录后沉默下调了II型肺泡细胞中IL-4刺激的eotaxin-3（CCL26）和其他CCR3配体的释放。

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摘要

Trafficking and inflammation in airway diseases are, in part, modulated by members of the CC chemokine family, eotaxin-1 (CCL11), eotaxin-2 (CCL24), and eotaxin-3 (CCL26), which transduce signals through their CCR3 receptor. In this context, we hypothesized that transfecting alveolar type II epithelial cells with CCR3-targeted siRNA or antisense (AS-ODN) sequences will downregulate cellular synthesis and release of the primary CCR3 ligands CCL26 and CCL24 and will modulate other CCR3 ligands. The human A549 alveolar type II epithelium-like cell culture model was used for transfection and subsequent effects on CCR3 agonists. siRNAs were particularly effective. PCR showed a 60-80% decrease in mRNA and immunoblots showed up to 75-84% reduction of CCR3 in siRNA treated cells. CCR3-siRNA treatments reduced IL-4 stimulated CCL26 release and constitutive CCL24 release by 65% and 80%, respectively. Release of four additional CCR3 agonists RANTES, MCP-2, MCP-3 and MCP-4 was also significantly reduced by CCR3-siRNA treatments of the alveolar type II cells. Activation of eosinophils, assessed as superoxide anion generation, was reduced when eosinophils were treated with supernatants of A549 cells pretreated with CCR3-targeted siRNAs or AS-ODNs. Collectively, the data suggest that post-transcriptional regulation of CCR3 receptors may be a potential therapeutic approach for interrupting proinflammatory signaling.
机译：气道疾病的贩运和炎症部分受CC趋化因子家族成员eotaxin-1（CCL11），eotaxin-2（CCL24）和eotaxin-3（CCL26）的调节，它们通过其CCR3受体转导信号。在这种情况下，我们假设用靶向CCR3的siRNA或反义（AS-ODN）序列转染II型肺泡上皮细胞将下调细胞合成和主要CCR3配体CCL26和CCL24的释放，并调节其他CCR3配体。使用人类A549 II型肺泡上皮样细胞培养模型进行转染，并随后对CCR3激动剂产生影响。 siRNA特别有效。 PCR显示在siRNA处理的细胞中，mRNA降低60-80％，免疫印迹显示CCR3降低高达75-84％。 CCR3-siRNA处理分别将IL-4刺激的CCL26释放和组成型CCL24释放降低了65％和80％。通过II型肺泡细胞的CCR3-siRNA处理，还显着减少了另外四种CCR3激动剂RANTES，MCP-2，MCP-3和MCP-4的释放。当将嗜酸性粒细胞用经CCR3靶向的siRNA或AS-ODN预处理的A549细胞上清液处理后，嗜酸性粒细胞的活化（以超氧阴离子的生成来评估）会降低。总体而言，数据表明CCR3受体的转录后调节可能是中断促炎信号传导的潜在治疗方法。

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