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目的：探讨Ｐ物质（ＳＰ）对嗜酸性粒细胞（Ｅｏｓ）粘附功能的调节作用及机制．方法：用收集５１Ｃｒ标记的白细胞分析法观察人Ｅｏｓ对培养的人脐带静脉血管内皮细胞（ＨＵＶＥＣ）的粘附作用．在实验中以不同浓度ＳＰ和ＳＰ＋血小板激活因子（ＰＡＦ）分别预处理Ｅｏｓ，观察其对经ＩＬ－１β活化的ＨＵＶＥＣ粘附性变化．以ＧＲ７１２５１（ＮＫ－１受体阻断剂）和抗ＣＤ１１ｂ作为干预因素，观察它们对ＳＰ＋ＰＡＦ作用的影响．此外，我们还以ＳＰ预刺激ＨＵＶＥＣ，观察其对经ＳＰ＋ＰＡＦ活化人Ｅｏｓ的粘附性变化．结果：单纯ＳＰ不能增加Ｅｏｓ对经ＩＬ－１β活化的ＨＵ－ＶＥＣ的粘附性，却能显著增加ＰＡＦ的促粘效应，这一作用呈剂量依赖性并且被ＧＲ７１２５１和抗ＣＤ１１ｂ所阻断，阻断率分别为２９．２％和５９．２％．ＳＰ预处理ＨＵＶＥＣ后，ＨＵＶＥＣ对ＳＰ＋ＰＡＦ活化的Ｅｏｓ的粘附性增强，也呈剂量依赖性，ＧＲ７１２５１对此有显著的抑制作用．结论：ＳＰ能促进ＰＡＦ对人Ｅｏｓ的粘附性，ＮＫ－１受体和ＣＤ１１ｂ可能参与这一过程；ＳＰ还能激活ＨＵＶＥＣ，使其对Ｅｏｓ的粘附作用增强．
Objective: To investigate the regulatory effect of substance P (SP) on the adhesion of eosinophils (Eos) and its mechanism. Methods: The adhesion of human Eos to cultured human umbilical vein endothelial cells (HUVECs) was observed by 51Cr-labeled leukocyte assay. In the experiment, Eos were pretreated with different concentrations of SP and SP + platelet activating factor (PAF) to observe the change of adhesion to HUVECs activated by IL-1β. The effects of GR71251 (NK-1 receptor blocker) and anti-CD11b as interventional factors on the effects of SP + PAF were observed. In addition, we also pre-stimulated HUVECs with SP and observed their adherence changes to Eos activated by SP + PAF. Results: SP alone could not increase the Eos adhesion to HU-VEC activated by IL-1β, but significantly increased the adhesion-promoting effect of PAF. This effect was dose-dependent and blocked by GR71251 and anti-CD11b The break rates were 29.2% and 59.2% respectively. After pretreatment of SP with HUVEC, the adhesion of HUVEC to SP + PAF-activated Eos was enhanced, also in a dose-dependent manner, and GR71251 had a significant inhibitory effect on this. CONCLUSION: SP can promote the adhesion of PAF to human Eos, and NK-1 receptor and CD11b may participate in this process. SP can also activate HUVEC to enhance its adhesion to Eos.