Mullol J, Baraniuk J N, Logun C, Benfield T, Picado C, Shelhamer J H
Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892, USA.
Neuropeptides. 1996 Dec;30(6):551-6. doi: 10.1016/s0143-4179(96)90038-4.
Endothelin (ET) is a powerful vasoconstrictor and bronchoconstrictor peptide that may be involved in the pathogenesis of bronchial asthma. We have investigated the effect of ET on the secretion of IL-6, IL-8, GM-CSF and G-CSF in a bronchial epithelial cell line (BEAS-2B). Incubation of BEAS-2B cells with ET-1 (10(-13) to 10(-7) M) for 4 h caused dose-related increases in the release of IL-8 (68% increase above control, P < 0.001) and IL-6 (43% increase above control, P < 0.001), compared to untreated control cells. After 48 h incubation, ET-1 also increased the release of IL-8 by 35% (P < 0.001) and GM-CSF by 38% (P < 0.01). ET-1 had no significant effect on G-CSF release. ET-1 did not induce cell proliferation at 24 or 48 h. Since ET-immunoreactive materials are expressed in epithelial cells in asthma, it is possible that ET-1 of epithelial origin may act in a paracrine or autocrine fashion on airway epithelial ET receptors to stimulate IL-8, IL-N6 and GM-CSF release. Thus, ET-1 may play a role in the regulation of the cytokine responses involved in inflammation of the airway mucosa.
内皮素（ET）是一种强效的血管收缩剂和支气管收缩剂肽，可能参与支气管哮喘的发病机制。我们研究了ET对支气管上皮细胞系（BEAS-2B）中白细胞介素-6（IL-6）、白细胞介素-8（IL-8）、粒细胞-巨噬细胞集落刺激因子（GM-CSF）和粒细胞集落刺激因子（G-CSF）分泌的影响。与未处理的对照细胞相比，用ET-1（10^(-13)至10^(-7) M）孵育BEAS-2B细胞4小时导致IL-8释放量呈剂量相关增加（比对照增加68%，P < 0.001）和IL-6释放量增加（比对照增加43%，P < 0.001）。孵育48小时后，ET-1还使IL-8释放量增加35%（P < 0.001），GM-CSF释放量增加38%（P < 0.01）。ET-1对G-CSF释放无显著影响。ET-1在24小时或48小时时未诱导细胞增殖。由于哮喘患者上皮细胞中表达有ET免疫反应性物质，上皮来源的ET-1有可能以旁分泌或自分泌方式作用于气道上皮ET受体，刺激IL-8、IL-6和GM-CSF释放。因此，ET-1可能在调节气道黏膜炎症相关的细胞因子反应中发挥作用。
