EICOSANOID FORMATION IN PULMONARY EPITHELIAL CELLS

呼吸道上皮细胞在呼吸道感染中起着重要作用。 肺的炎症作用由生物活性的形成 像二十烷类这样的分子。上皮细胞作为一种 气管和支气管的气液屏障，是 包括粘液在内的分泌物。类维A酸类化合物是维持 粘液纤毛表型。缺乏维甲酸会导致 在几种肺部疾病中观察到的鳞状化生。 粘液纤毛细胞产生高水平的PGE2，Express高 CPLA2和PGHS-2水平。该气-液界面系统具有 已经成功地扩展到人的支气管上皮细胞。这个 人细胞低代谢花生四烯酸为前列腺素 与老鼠细胞形成对比。在缺乏维甲酸的情况下， 未检测到15-脂氧合酶和PGHS-2。有了维甲酸， 这些细胞分化为粘液纤毛细胞和Western和 Northern分析表明，存在高水平的 15-脂氧合酶。在IL-4中孵育极大地促进了 15-LO表达增加而对COX-2无影响 表情。IL-4对粘蛋白的分泌也有抑制作用，且有一定的时程 这表明15-LO可能下调粘蛋白的分泌。 然而，还需要更多的实验来确定 15-LO调节粘蛋白的分泌。这些研究表明， 15-脂氧合酶在人肺炎性疾病中的作用 回应。

The airway epithelium plays an important role in the inflammatory role of the lung by the formation of bioactive molecules such as eicosanoids. The epithelium serves as an air-liquid barrier for the trachea and bronchi and is a source of secretions including mucin. Retinoids are essential for maintaining the muco-cilliary phenotype. The absence of retinoids leads to squamous metaplasia which is observed in several lung diseases. Muco-cilliary cells produced high levels of PGE2, Express high levels of cPLA2 and PGHS-2. The air-liquid interface system has been successfully extended to human bronchial epithelial cells. The human cells poorly metabolize arachidonic acid to prostaglandins in contrast to the rat cells. In the absence of retinoids, 15-Lipoxygenase and PGHS-2 were not detected. With retinoids, these cells differentiate to muco-cilliary cells and Western and Northern analysis indicated the presence of high levels of the 15-lipoxygenase. Incubation in IL-4 dramatically furthers the increase in expression of 15-LO with no effect on COX-2 expression. IL-4 also inhibited mucin secretion with a time course which suggests 15-LO may down regulate mucin secretion. However, additional experiments are required to determine if 15-LO modulates mucin secretion. These studies indicate an importance of 15-Lipoxygenase in human lung inflammatory responses.