INDUCTION OF CYTOKINE GENE EXPRESSION IN RESPIRATORY EPITHELIAL CELLS

气道上皮细胞在调节气道炎症中的作用 本文研究了已经发现，TNF-α和IL-1 β是 能够刺激IL-6、IL-8和G-CSF的基因表达， 人支气管上皮细胞系随后的研究 证明了神经肽VIP能够诱导 产生IL-6和IL-8。此外，自分泌效应物， 内皮素-1能够诱导IL-6和IL-8的产生， 而不是G-CSF或GM-CSF。气道上皮细胞上有细胞 表面，TNF-α的p55受体，以及I型和II型 IL-1 β受体。蛋白激酶C的激活剂，诱导 溶解并释放到TNF p55受体的介质中。 类似地，IL-1 II型受体，可能不 参与信号转导的蛋白质也可以被溶解， 响应细胞因子刺激而释放到培养基中。 这两种受体增溶事件可能是 上皮细胞对炎症刺激的反应，可能是 细胞因子对上皮细胞作用的阴性对照。这个项目 可能会让我们对促炎细胞因子的作用有新的认识， 在上皮细胞上。

The role of the airway epithelium in modulatory airway inflammation has been studied. It has been found that TNF-alpha and IL-1 beta are capable of stimulating gene expression of IL-6, IL-8, and G-CSF in a human bronchial epithelial cell line. Subsequent studies have demonstrated that the neuropeptide VIP is capable of inducing the production of IL-6 and IL-8. Further, the autocrine effector, Endothelin-1 is capable of inducing the production of IL-6, and IL-8, but not G-CSF or GM-CSF. Airway epithelial cells have on the cell surface, the p55 receptor for TNF-alpha, and the Type I and Type II receptors for IL-1 beta. Activators of protein kinase C, induce the solubilization and release into the medium of the TNF p55 receptor. Similarly, the IL-1 Type II receptor, which presumably does not participate in signal transduction may also be solubilized and released into the culture medium in response to cytokine stimulation. Both of these events of receptor solubilization may be a part of the epithelial response to inflammatory stimuli and may be integral to the negative control of cytokine effects on epithelial cells. This project may allow for new insight into the effect of proinflammatory cytokine on epithelial cells.