SummaryBackgroundActivation of platelets and expression of adhesion molecules (e.g. CD62P and CD63) which mediate interactions between platelets and other cells may be important in the pathogenesis of aspirin‐sensitive asthma.ObjectiveTo determine the expression of CD62P and CD63 on platelets from aspirinsensitive asthmatic (ASA +), aspirin‐tolerant asthmatic (ASA‐) and normal subjects and to assess the modulatory effect of aspirin on platelet CD62P and CD63 expression following stimulation with either platelet‐activating factor (PAF), arachidonic acid (AA) or collagen (COL).MethodsPlatelet‐rich plasma was obtained from 10 ASA +, 10 ASA—and 10 normal control subjects, and expression of CD62P and CD63 was measured by flow cytometry. Platelets were stimulated with PAF (10, 80 nM), AA (0.1, 1 mM) or COL (80, 800 μg/mL) with or without aspirin (concentration range 0.4–4 mg/mL).ResultsIn the absence of aspirin, CD62P expression induced by AA and COL was greater in ASA+ patients compared with control subjects (P<0.001) while CD62P expression with PAF, AA and COL was reduced in ASA—when compared wilh ASA+ and control subjects (P<0.001). CD63 expression with PAF and AA was reduced in both ASA+ and ASA‐ patients compared with control subjects (P<0.001). Aspirin inhibited the expression of both CD62P and CD63 after agonist stimulatitin. Greater inhibition of CD62P expression was observed in ASA+ compared with ASA‐ patients (P<0.001) and normal subjects (P<0.05) while greater inhibition of CD63 expression was observed in normal subjects compared with both ASA+ and ASA‐ patients (P<0.05). In ASA+ patients and normal subjects, stimulation with PAF and COL resulted in only one platelet population while in contrast with 1 mM AA two populations were observed.ConclusionsFnhanced AA‐ and collagen‐induced platelet CD62P expression in ASA+patients compared with normal subjects and greater inhibition by aspirin of CD62P expression in ASA+ may be relevant to the pathogenesis of this syndrome. Reduced expression of CD62P and CD63 in platelets of ASA‐ patients following stimulation with PAF and AA may also have implications for the role of platelets and these mediators in the pathogene
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机译：摘要背景介导血小板和其他细胞之间相互作用的血小板活化和粘附分子（例如 CD62P 和 CD63）的表达可能在阿司匹林敏感性哮喘的发病机制中很重要。目的探讨阿司匹林活化因子（PAF）、花生四烯酸（AA）或胶原蛋白（COL）刺激后阿司匹林对哮喘（ASA+）、阿司匹林耐受哮喘（ASA‐）和正常受试者血小板CD62P和CD63表达的调节作用。方法取10例ASA+、10例ASA—和10例正常对照受试者的富血小板血浆，采用流式细胞术检测CD62P和CD63的表达。用PAF（10,80nM），AA（0.1,1mM）或COL（80,800μg/ mL）刺激血小板，联合或不联合阿司匹林（浓度范围为0.4–4mg/mL）。结果在无阿司匹林的情况下，ASA+患者AA和COL诱导的CD62P表达高于对照组（P<0.001），而ASA+组CD62P与PAF、AA和COL的表达率降低（P<0.001）。与对照组相比，ASA+和ASA-患者的CD63表达与PAF和AA均降低（P<0.001）。阿司匹林在激动剂刺激素后抑制CD62P和CD63的表达。与ASA患者（P<0.001）和正常受试者（P<0相比，ASA+对CD62P表达的抑制更大。05）与ASA+和ASA-患者相比，正常受试者对CD63表达的抑制更大（P<0.05）。在 ASA+ 患者和正常受试者中，PAF 和 COL 刺激仅导致一个血小板群，而与 1 mM AA 相比，观察到两个血小板群。结论与正常患者相比，ASA+患者AA和胶原诱导的血小板CD62P表达增强，阿司匹林对ASA+中CD62P表达的抑制更大，可能与该综合征的发病机制有关。在PAF和AA刺激后，ASA患者的血小板中CD62P和CD63的表达降低也可能对血小板和这些介质在病原体中的作用产生影响
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