INDUCTION OF CYTOKINE GENE EXPRESSION IN RESPIRATORY EPITHELIAL CELLS

呼吸道上皮细胞在调节气道炎症中的作用 已被研究过。已发现肿瘤坏死因子-α和白介素1-β是 能刺激IL-6、IL-8和G-CSF的基因表达 人支气管上皮细胞系。随后的研究发现 证明神经肽VIP能够诱导 IL-6和IL-8的产生。此外，自分泌效应器， 内皮素-1能够诱导IL-6和IL-8的产生， 但不是G-CSF或GM-CSF。呼吸道上皮细胞上有细胞 表面，肿瘤坏死因子-α的p55受体，以及I型和II型 IL-1β受体。蛋白激酶C的激活剂，诱导 增溶和释放到介质中的肿瘤坏死因子p55受体。 同样，IL-1II型受体，它可能不会 参与信号转导也可能被溶解和 在细胞因子刺激下释放到培养基中。 这两个受体增溶事件可能都是 上皮细胞对炎性刺激的反应可能是 细胞因子对上皮细胞影响的负性控制。这个项目 可能会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.