1. The effect of the selective type 4 phosphodiesterase (PDE 4) inhibitor rolipram on human eosinophil activation and migration mediated by eotaxin was investigated. 2. Studies were performed with human freshly isolated eosinophils from peripheral blood of healthy donors by a magnetic cell separation (MACS) technique to a purity > 99%. To test the effect of rolipram, eosinophils were stimulated with recombinant human eotaxin and the cell surface activation markers CD11b and L-selectin were analysed by flow cytometry. Furthermore, eotaxin mediated eosinophil migration was measured in a transendothelial chemotaxis assay. 3. Our results indicate that rolipram inhibited eotaxin-induced CD11b up-regulation up to 60.6 +/- 7.6% at the highest tested dose (10 microM), whereas transendothelial chemotaxis was partially inhibited reaching a plateau of approx. 30% at a rolipram concentration of 0.1 microM. 4. We conclude that the selective PDE 4 inhibitor rolipram decreases eotaxin mediated eosinophil activation, an observation that may contribute to elucidate the mechanism by which PDE 4 inhibitors reduce antigen-induced eosinophil infiltration in different animal models of allergic inflammation.

译文

1.研究了选择性4型磷酸二酯酶 (PDE 4) 抑制剂罗利普兰对eotaxin介导的人嗜酸性粒细胞活化和迁移的影响。2.研究是通过磁性细胞分离 (MACS) 技术从健康供体的外周血中分离的人新鲜嗜酸性粒细胞进行的,其纯度> 99%。为了测试罗利普兰的作用,用重组人嗜酸性粒细胞趋化因子刺激嗜酸性粒细胞,并通过流式细胞术分析细胞表面活化标记物CD11b和L-选择素。此外,在跨内皮趋化试验中测量了eotaxin介导的嗜酸性粒细胞迁移。3.我们的结果表明,在最高测试剂量 (10微米) 下,罗利普兰抑制eotaxin诱导的CD11b上调高达60.6 +/- 7.6%,而内皮细胞的趋化性被部分抑制,达到约。在0.1微米的罗利普拉姆浓度下30%。4.我们得出的结论是,选择性PDE 4抑制剂rolipram降低了eotaxin介导的嗜酸性粒细胞活化,这一观察结果可能有助于阐明PDE 4抑制剂在不同的过敏性炎症动物模型中减少抗原诱导的嗜酸性粒细胞浸润的机制。

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