1. Recent evidence has implicated eosinophils in the inhibition of allergen-induced rat pleurisy, but the mechanism of this negative modulation is not completely understood. This study was undertaken in order to define the potential role of prostaglandins in this phenomenon. 2. Wistar rats were actively sensitized by subcutaneous injection of a mixture of ovalbumin and AI(OH)3 and challenged with an intrapleural (i.pl.) injection of ovalbumin (12 micrograms/cavity) 14 days later. 3. Analysis of the pleural fluid effluent revealed a massive mast cell degranulation and plasma protein extravasation 4 h post-challenge. We confirmed that concurrently with selective pleural fluid eosinophilia caused by platelet-activating factor (PAF), the pleural cavity became hyporesponsive to allergen-induced protein exudation and to the parallel reduction in the number of intact mast cells. 4. These hyporesponsive animals presented a significant augmentation in the pleural effluent level of prostaglandin E2 (PGE2), which increased with increasing numbers of eosinophils in the pleural cavity. Furthermore, pretreatment with either indomethacin or aspirin failed to modify allergen-induced exudation but reversed the exudatory hyporesponsiveness associated with eosinophil recruitment. 5. Allergic exudation was clearly down-regulated by the following pretreatments(i) PGE2 (10 micrograms/cavity, i.pl.) plus rolipram (40 micrograms/cavity, i.pl.), (ii) misoprostol (200 micrograms kg-1, p.o.) or (iii) dibutyryl cyclic AMP (80 micrograms/cavity, i.pl.). 6. We conclude that prostaglandins may be implicated in the eosinophil-mediated inhibition of allergic pleurisy, probably acting via cyclic AMP signalling pathway activation.

译文

1.最近的证据表明嗜酸性粒细胞可以抑制变应原诱导的大鼠胸膜炎,但这种负调节的机制尚不完全清楚。进行这项研究是为了确定前列腺素在这种现象中的潜在作用。2. Wistar大鼠通过皮下注射卵白蛋白和AI(OH)3的混合物积极致敏,并在14天后用胸膜内 (i.pl.) 注射卵白蛋白 (12微克/腔) 攻击。3.对胸膜液流出物的分析显示,攻击后4小时,肥大细胞大量脱粒和血浆蛋白外渗。我们证实,在血小板活化因子 (PAF) 引起的选择性胸水嗜酸性粒细胞增多的同时,胸膜腔对变应原诱导的蛋白渗出和完整肥大细胞数量的平行减少具有低反应性。4.这些低反应性动物的胸膜流出物中前列腺素E2 (PGE2) 的水平显着增加,并且随着胸膜腔中嗜酸性粒细胞的增加而增加。此外,用吲哚美辛或阿司匹林进行预处理未能改变过敏原诱导的渗出,但逆转了与嗜酸性粒细胞募集相关的渗出性低反应性。5.通过以下预处理 (i) PGE2 (10微克/腔,i.pl.) 加罗利普兰 (40微克/腔,i.pl.),(ii) 米索前列醇 (200微克kg-1,p.o.) 或 (iii) 二丁酰基环状AMP (80微克/腔,i.pl.)。6.我们得出的结论是,前列腺素可能与嗜酸性粒细胞介导的过敏性胸膜炎抑制有关,可能通过环状AMP信号通路激活起作用。

+1
+2
100研值 100研值 ¥99课程
检索文献一次
下载文献一次

去下载>

成功解锁2个技能,为你点赞

《SCI写作十大必备语法》
解决你的SCI语法难题!

技能熟练度+1

视频课《玩转文献检索》
让你成为检索达人!

恭喜完成新手挑战

手机微信扫一扫,添加好友领取

免费领《Endnote文献管理工具+教程》

微信扫码, 免费领取

手机登录

获取验证码
登录