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[血小板在过敏性炎症中的作用]

[The role of thrombocytes in allergic inflammation].

作者信息

Jovisić Z, Bogić M, Rasković S, Perić-Popadić A

机构信息

Institute for Allergology and Immunology, Clinical Centre of Serbia, Belgrade.

出版信息

Srp Arh Celok Lek. 1998 Jan-Feb;126(1-2):54-60.

PMID:9525084
Abstract

The platelet has traditionally been associated with haemostasis. Participation of platelets in defence mechanisms is presentiment by the knowledge that primary haemostasis may be phylogenetic vestige retained from the behaviour of primitive leukocytes. Platelets have the ability to undergo shape change with pseudopod formation, chemotaxis, diapedesis, and phagocytose. Platelets contain a wide range highly potent inflammatory factors that are capable of inducing or augmenting certain inflammatory responses. Different surface molecules have been detected on the plasma membrane, highlight the platelets ability to bind a variety of biologic surfaces, including those of other cells, resulting in close apposition of platelets and their targets. They can interact with parasites, viruses and bacteria. Studies from several groups suggest an important role of the platelet in allergic processes. Platelets possess receptor for immunoglobulin E. Numerous clinical reports are describing the modification of biologic activity of platelets from allergic patients as compared to healthy subjects. The incidence of abnormal platelet responsiveness is in higher among patients having high serum IgE titres. Platelet depletion decreased the anaphylactic response and protects against the lethal consequences of the antigen provocation. Evidence now exists in support of primary role of the platelet in the pathogenesis of bronchial asthma. Platelets can participate in allergic asthma by acting as inflammatory cells, by releasing spasmogens and by interacting with other inflammatory cells. Thrombocytopenia and the increased plasma levels of platelet-derived markers occurred in parallel with bronchoconstriction induced by antigen provocation of allergic astmatics. Platelet depletion inhibits the ability of antigen to induce late onset airways obstruction and airway hyperresponsiveness. Platelet apheresis in human resulted in a positive clinical effect. Platelets respond to aspirin or other NSAIDs in acetyl salicylic acid sensitive asthmatics and these findings provide further evidence for role of the platelet in this form of bronchial asthma.

摘要

传统上认为血小板与止血有关。血小板参与防御机制这一观点是基于这样的认识:初级止血可能是从原始白细胞行为保留下来的系统发育遗迹。血小板能够发生形态变化,形成伪足、趋化、穿出血管壁并进行吞噬。血小板含有多种高效的炎症因子,能够诱导或增强某些炎症反应。在质膜上已检测到不同的表面分子,这突出了血小板与多种生物表面结合的能力,包括其他细胞的表面,从而导致血小板与其靶标紧密相邻。它们可以与寄生虫、病毒和细菌相互作用。多个研究小组的研究表明血小板在过敏过程中起重要作用。血小板拥有免疫球蛋白E受体。众多临床报告描述了与健康受试者相比,过敏患者血小板生物活性的改变。血清IgE滴度高的患者中血小板反应异常的发生率更高。血小板减少可降低过敏反应,并预防抗原激发的致命后果。现在有证据支持血小板在支气管哮喘发病机制中起主要作用。血小板可通过作为炎症细胞、释放致痉物质以及与其他炎症细胞相互作用来参与过敏性哮喘。血小板减少症和血小板衍生标志物的血浆水平升高与过敏性哮喘患者抗原激发诱导的支气管收缩同时出现。血小板减少可抑制抗原诱导迟发性气道阻塞和气道高反应性的能力。人体血小板单采术产生了积极的临床效果。在对乙酰水杨酸敏感的哮喘患者中,血小板对阿司匹林或其他非甾体抗炎药有反应,这些发现为血小板在这种形式的支气管哮喘中的作用提供了进一步的证据。

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