INTERLEUKIN-1-MEDIATED RELEASE OF INTERLEUKIN-8 BY ASBESTOS-STIMULATED HUMAN PLEURAL MESOTHELIAL CELLS
INTERLEUKIN-1-MEDIATED RELEASE OF INTERLEUKIN-8 BY ASBESTOS-STIMULATED HUMAN PLEURAL MESOTHELIAL CELLS
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DOI：
10.1165/ajrcmb.10.3.8117443
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发表时间：
1994-03-01
影响因子：
6.4
通讯作者：
JOHNSON, AR
中科院分区：
文献类型：
--
作者：
GRIFFITH, DE;MILLER, EJ;JOHNSON, AR
对吸入石棉的胸膜肺反应经常涉及炎症和肺细胞释放各种细胞因子。其中，从间皮释放的白介素 8 (IL-8) 可以通过将中性粒细胞吸引到胸膜腔来加剧胸膜炎症。我们使用人胸膜间皮细胞 (HPMC) 培养物来研究石棉和细胞因子产生 IL-8 的机制。浓度低至 5 μg/ml 的铁石棉、温石棉或青石棉悬浮液可在 37 摄氏度孵育 6 小时期间增强 HPMC 中 IL-8 的释放。石棉处理的 HPMC 的电子显微镜显示，细胞贪婪地吞噬每种不同类型的石棉纤维。两种促炎细胞因子白介素 1 α (IL-1 α) 和肿瘤坏死因子或肿瘤坏死因子可在 2 小时内增强 IL-8 的释放，并在 6 小时后产生更大的效果。通过酶联免疫吸附测定测量IL-8的释放，并通过人中性粒细胞的趋化性评估细胞因子的功能活性。 HPMC 上清液中 IL-8 的身份通过 IL-8 抗体的吸收来确定。 HPMC 与 IL-1 受体拮抗剂 (IL-1ra) 预孵育可显着减少铁石棉或青石棉刺激后 IL-8 的释放。我们得出结论，HPMC 响应石棉刺激而释放 IL-8，并且该反应部分由 IL-1（主要以 IL-1 α 的形式）介导。
The pleuropulmonary response to inhaled asbestos frequently involves inflammation and release of various cytokines from lung cells. Among these, interleukin-8 (IL-8) released from the mesothelium could augment inflammation of the pleura by attracting neutrophils to the pleural space. We used cultures of human pleural mesothelial cells (HPMC) to examine the mechanism of IL-8 production by asbestos and cytokines. Suspensions of amosite, chrysotile, or crocidolite asbestos in concentrations as low as 5 mu g/ml enhanced release of IL-8 from HPMC during 6 h of incubation at 37 degrees C. Electron microscopy of asbestos-treated HPMC showed that the cells avidly engulfed each of the different types of asbestos fibers. Two proinflammatory cytokines, interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-or, enhanced IL-8 release within 2 h and had an even greater effect after 6 h. Release of IL-8 was measured by an enzyme-linked immunosorbent assay, and functional activity of the cytokine was assessed by chemotaxis of human neutrophils. Identity of IL-8 in HPMC supernatants was established by absorption with an antibody to IL-8. Preincubation of HPMC with IL-1 receptor antagonist (IL-1ra) significantly decreased release of IL-8 after stimulation with amosite or crocidolite asbestos. We conclude that HPMC release IL-8 in response to asbestos stimulation and that the response is, in part, mediated by IL-1, mainly in the form of IL-1 alpha.