Eosinophil recruitment into guinea pig lungs after PAF-acether and allergen administration. Modulation by prostacyclin, platelet depletion, and selective antagonists.
Eosinophil recruitment into guinea pig lungs after PAF-acether and allergen administration. Modulation by prostacyclin, platelet depletion, and selective antagonists.
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PAF-乙醚和过敏原给药后，嗜酸性粒细胞募集到豚鼠肺中。
DOI：
10.1164/ajrccm/137.4.948
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
B. Vargaftig
中科院分区：
文献类型：
--
作者：
A. Lellouch‐Tubiana;J. Lefort;Marie;André Pfister;B. Vargaftig
豚鼠静脉注射PAF-醋酸酯可诱导支气管收缩、低血压、血管内血小板聚集、内皮破坏以及血小板和中性粒细胞渗出。这些效应之后1小时内出现嗜酸性粒细胞浸润至支气管壁，这也在被动致敏豚鼠给予抗原后观察到。支气管收缩和嗜酸性粒细胞浸润是哮喘的两个主要特征，选择性支气管嗜酸性粒细胞增多是晚期哮喘反应的特征。我们比较了PAF-醋酸酯静脉注射后6和24 h的组织学效应与用作哮喘模型的实验性被动过敏性休克的组织学效应。PAF-醋酸酯或抗原（卵清蛋白）给药后6小时，观察到显著的肺嗜酸性粒细胞浸润，特别是在支气管壁中，以及支气管腔内含有嗜酸性粒细胞的粘液栓。24小时后，支气管上皮发生粘膜化生，上皮脱落。当使用无活性代谢物lyso-PAF时，未观察到这些作用。我们的研究结果完全同意的建议，嗜酸性粒细胞介导的病理生理支气管哮喘和释放有毒物质的呼吸道上皮。两种PAF-乙酸酯拮抗剂（BN 52021和WEB 2086）可防止PAF-乙酸酯和抗原引发的嗜酸性粒细胞浸润。当在抗血小板血清或前列环素后向豚鼠注射PAF-乙酸酯或卵清蛋白时，嗜酸性粒细胞浸润显著减少，表明血小板或另一种腺苷酸环化酶敏感细胞对随后的PAF-乙酸酯诱导的嗜酸性粒细胞浸润是重要的。我们的研究结果支持PAF-醋酸酯在过敏性哮喘实验模型中的重要作用。
Intravenous administration of PAF-acether to the guinea pig induces bronchoconstriction, hypotension, intravascular platelet aggregation, endothelial disruption, and platelet and neutrophil diapedesis. These effects are followed within 1 h by an eosinophilic infiltration into the bronchial walls, which was also noted after the administration of antigen to passively sensitized guinea pigs. Bronchoconstriction and eosinophil infiltration are 2 major features of asthma, and selective bronchial eosinophilia characterizes late asthmatic reactions. We compared the histologic effects of PAF-acether 6 and 24 h after its intravenous injection with those of experimental passive anaphylactic shock, which is used as a model for asthma. Six hours after PAF-acether or antigen (ovalbumin) administration, a marked lung eosinophil infiltration, particularly in the bronchial walls, was noted, together with mucous plugs containing eosinophils in the bronchial lumen. Epithelial desquamation was followed after 24 h by mucous metaplasia of the bronchial epithelium. These effects were not observed when the inactive metabolite lyso-PAF was used. Our results agree fully with the suggestion that the eosinophil mediates the pathophysiology of bronchial asthma and releases materials toxic for the respiratory epithelium. Two PAF-acether antagonists (BN 52021 and WEB 2086) prevented the eosinophil infiltration triggered by PAF-acether and by antigen. When PAF-acether or ovalbumin were injected into guinea pigs after antiplatelet serum or prostacyclin, the eosinophil infiltration was significantly reduced, suggesting that platelets or another adenylate cyclase-sensitive cell are important for the subsequent PAF-acether-induced eosinophil infiltration. Our results support an essential role for PAF-acether in an experimental model of allergic asthma.
早期和晚期哮喘反应期间嗜酸性粒细胞趋化活性和中性粒细胞趋化活性的产生和部分表征。
DOI：
10.1016/s0091-6749(86)80077-x
发表时间：
1986
期刊：
The Journal of allergy and clinical immunology
影响因子：
--
作者：
Metzger,WJ;Richerson,HB;Wasserman,SI
通讯作者：
Wasserman,SI