TWEAK/Fn14 interaction stimulates human bronchial epithelial cells to produce IL-8 and GM-CSF
TWEAK/Fn14 interaction stimulates human bronchial epithelial cells to produce IL-8 and GM-CSF
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DOI：
10.1016/j.bbrc.2004.04.036
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发表时间：
2004-05-28
影响因子：
3.1
通讯作者：
Nakao, A
中科院分区：
文献类型：
--
作者：
Xu, HR;Okamoto, A;Nakao, A
肿瘤坏死因子样弱凋亡诱导因子（TWEAK）是肿瘤坏死因子（TNF）家族的成员，是一种多功能细胞因子，调节细胞增殖、血管生成、炎症和凋亡。在这项研究中，我们研究了TWEAK对人支气管上皮细胞的影响。人支气管上皮细胞系BEAS 2B表达TWEAK受体，成纤维细胞生长因子诱导型14（Fn 14），并在TWEAK刺激后以剂量依赖性方式产生IL-8和GM-CSF，其被抗Fn 14阻断抗体废除。TWEAK诱导IkappaB α和BAY 11 -7082（一种IkappaB α的选择性抑制剂）的磷酸化。磷酸化，抑制BEAS 2B细胞的TWEAK诱导的IL-8和GM-CSF产生。此外，原代培养的人支气管上皮细胞在TWEAK刺激后也表达Fn 14并产生IL-8和GM-CSF。总的来说，TWEAK通过Fn 14刺激人支气管上皮细胞产生IL-8和GNI-CSF。由于IL-8和GNI-CSF与炎症状态相关，这些结果表明TWEAK/Fn 14相互作用可能在气道炎症反应中起重要作用。(C)2004年爱思唯尔公司All rights reserved.
TNF-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor (TNF) family, is a multifunctional cytokine that regulates cellular proliferation, angiogenesis, inflammmation, and apoptosis. In this study, we investigated the effect of TWEAK on human bronchial epithelial cells. A human bronchial epithelial cell line, BEAS2B, expressed a TWEAK receptor, fibroblast growth factor-inducible 14 (Fn14), and produced IL-8 and GM-CSF upon TWEAK stimulation in a dose-dependent manner, which was abrogated by anti-Fn14 blocking antibody. TWEAK induced phosphorylation of IkappaBalpha and BAY11-7082, a selective inhibitor of IkappaBalpha. phosphorylation, inhibited the TWEAK-induced IL-8 and GM-CSF production by BEAS2B cells. Moreover, primary Cultured human bronchial epithelial cells also expressed Fn14 and produced IL-8 and GM-CSF upon TWEAK stimulation. Collectively, TWEAK stimulated human bronchial epithelial cells to produce IL-8 and GNI-CSF through Fn14. Because IL-8 and GNI-CSF are associated with inflammatory conditions, these results suggest that TWEAK/Fn14 interaction may play sonic roles in airway inflammatory responses. (C) 2004 Elsevier Inc. All rights reserved.