PLATELET ACTIVATION IN THE LUNG AFTER ANTIGEN CHALLENGE IN A MODEL OF ALLERGIC-ASTHMA
PLATELET ACTIVATION IN THE LUNG AFTER ANTIGEN CHALLENGE IN A MODEL OF ALLERGIC-ASTHMA
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DOI：
10.1164/ajrccm/145.3.571
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发表时间：
1992-03-01
期刊：
影响因子：
--
通讯作者：
LIU, MC
中科院分区：
文献类型：
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作者：
AVERILL, FJ;HUBBARD, WC;LIU, MC
本研究的目的是调查抗原攻击后血小板是否被激活并在人肺中释放其产物。 使用亚节段抗原激发作为哮喘模型，在豚草抗原激发前（基线）以及豚草抗原激发后 5 分钟和 19 小时，对豚草过敏性哮喘受试者的支气管肺泡灌洗液中的 α 颗粒产物、血小板因子 4 (PF4) 和 β-血栓球蛋白 (β-TG) 进行测定。 用生理盐水激发的气道段用作对照。 抗原激发后五分钟，BAL 液中的血小板产物水平未从基线或生理盐水对照水平升高。 然而，抗原攻击 19 小时后，发现 BAL 液中的血小板产物增加了 10 倍。 抗原攻击后 19 小时，平均 PF4 水平从基线和盐水对照值增加至 7.2 ng/ml (p < 0.05)，低于 1.0。 Beta-TG 从低于 1.0 的基线和对照水平增加至 6.6 ng/ml (p < 0.05)。 PF4 和 beta-TG 的升高彼此高度相关 (r = 0.98, p < 0.0001)。 19小时反应期间血小板产物的水平与白蛋白、激肽、前列腺素6-酮-PGF1-α、PGE2和PGF2-α以及嗜酸性粒细胞衍生蛋白、嗜酸性粒细胞衍生神经毒素和嗜酸性粒细胞过氧化物酶相关。 我们的结论是，肺部血小板活化是对抗原攻击的晚期炎症反应的一个特征，并且血小板可能在过敏性炎症和哮喘中发挥重要作用。
The purpose of this study was to investigate whether platelets are activated and release their products in the human lung after antigen challenge. Using subsegmental antigen challenge as a model of asthma, bronchoalveolar lavage fluids from ragweed-allergic asthmatic subjects were assayed for the alpha granule products, platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG), prior to challenge (baseline) and at 5 min and 19 h after challenge with ragweed antigen. Airway segments challenged with normal saline were used as controls. Five minutes after antigen challenge, levels of platelet products in BAL fluid were not elevated from baseline or normal saline control levels. However, 19 h after antigen challenge, a 10-fold increase in platelet products in BAL fluids was found. The mean PF4 levels increased from baseline and saline control values of less than 1.0 to 7.2 ng/ml (p < 0.05) 19 h after antigen challenge. Beta-TG increased from baseline and control levels of less than 1.0 to 6.6 ng/ml (p < 0.05). Elevations in PF4 and beta-TG were highly correlated with each other (r = 0.98, p < 0.0001). Levels of platelet products during the 19-h response correlated with albumin, with kinins, with the prostaglandins 6-keto-PGF1-alpha, PGE2, and PGF2-alpha, and with the eosinophil-derived proteins, eosinophil-derived neurotoxin and eosinophil peroxidase. We conclude that platelet activation in the lung is a feature of the late inflammatory response to antigen challenge and that platelets may play an important role in allergic inflammation and asthma.