Schäfer D, Lindenthal U, Wagner M, Bölcskei P L, Baenkler H W
Department of Allergology, University of Erlangen-Nuremberg, Germany.
Thorax. 1996 Sep;51(9):919-23. doi: 10.1136/thx.51.9.919.
Eicosanoids such as prostaglandin E2 (PGE2), thromboxane A2 (TXA2), and peptidoleukotrienes (pLT) are known to be biologically highly active lipid mediators, especially in human lung epithelium. PGE2 is thought to have mostly bronchoprotective effects, whereas pLT and TXA2 are bronchoconstrictive. This study was undertaken to assess the release and interaction of eicosanoids in human bronchial biopsy specimens of normal and inflamed mucosa.
Bronchial biopsy specimens were obtained from 16 patients, seven controls without signs of inflammation and nine patients with severe inflammatory processes in the epithelium. The release of pLT, TXA2 (measured as TXB2), and PGE2 was investigated using a "functional in vitro test" and the addition of several stimuli.
Specimens incubated with arachidonic acid released higher amounts of pLT, TXB2, and PGE2 than unstimulated specimens. Preincubation with PGE2 revealed significant inhibition of arachidonic acid-induced release of pLT and TXB2 (> 50%). The inhibitory effect was higher in normal than in inflamed epithelium.
Exogenous PGE2 has inhibitory effects on the release of pLT and TXB2 in human bronchial biopsy specimens. This finding could explain the bronchoprotective effect of inhaled PGE2 in normal subjects and asthmatic subjects as direct eicosanoid interactions. It also supports the concept of PGE2 as a bronchoprotective endogenous substance. The complex effects of PGE2 as a modulating mediator in inflammation may be worth investigating.
类花生酸如前列腺素E2（PGE2）、血栓素A2（TXA2）和肽白三烯（pLT）是已知的生物活性很高的脂质介质，尤其在人肺上皮细胞中。PGE2被认为主要具有支气管保护作用，而pLT和TXA2具有支气管收缩作用。本研究旨在评估正常和炎症黏膜的人支气管活检标本中类花生酸的释放及相互作用。
从16例患者获取支气管活检标本，其中7例为无炎症迹象的对照者，9例为上皮有严重炎症过程的患者。使用“体外功能试验”并添加多种刺激物来研究pLT、TXA2（以TXB2衡量）和PGE2的释放。
与花生四烯酸孵育的标本比未刺激的标本释放出更多的pLT、TXB2和PGE2。用PGE2预孵育显示花生四烯酸诱导的pLT和TXB2释放受到显著抑制（>50%）。正常上皮中的抑制作用高于炎症上皮。
外源性PGE2对人支气管活检标本中pLT和TXB2的释放具有抑制作用。这一发现可以解释吸入PGE2在正常人和哮喘患者中的支气管保护作用是作为类花生酸的直接相互作用。它也支持PGE2作为支气管保护内源性物质的概念。PGE2作为炎症中调节介质的复杂作用可能值得研究。
