Endoscopic implantation of medical devices for the treatment of lung diseases, including airway stents, unidirectional valves and coils, is readily used to treat central airway disease and emphysema. However, granulation and fibrotic tissue formation impairs treatment effectiveness. To date little is known about the interaction between implanted devices, often made from metals, such as nickel, titanium or nitinol, and cells in the airways. Here, we study the response of lung epithelial cells and fibroblasts to implant device materials. The adhesion and proliferation of bronchial epithelial cells and lung fibroblasts upon exposure to 10 × 3 × 1 mm pieces of nickel, titanium or nitinol is examined using light and scanning electron microscopy. Pro-inflammatory cytokine mRNA expression and release, signaling kinase activity and intracellular free radical production are assessed. Nitinol, and to a lesser extent nickel and titanium, surfaces support the attachment and growth of lung epithelial cells. Nitinol induces a rapid and significant alteration of kinase activity. Cells directly exposed to nickel or titanium produce free radicals, but those exposed to nitinol do not. The response of lung epithelial cells and fibroblasts depends on the metal type to which they are exposed. Nitinol induces cellular surface growth and the induction of kinase activity, while exposure of lung epithelial cells to nickel and titanium induces free radical production, but nitinol does not.

Graphical Abstract

中文翻译：

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主机与设备的相互作用：肺上皮细胞和成纤维细胞接触镍、钛或镍钛诺会影响增殖、活性氧的产生和细胞信号传导

内窥镜植入治疗肺部疾病的医疗器械，包括气道支架、单向阀和线圈，很容易用于治疗中央气道疾病和肺气肿。然而，肉芽和纤维化组织的形成会损害治疗效果。迄今为止，人们对植入装置（通常由镍、钛或镍钛诺等金属制成）与气道细胞之间的相互作用知之甚少。在这里，我们研究肺上皮细胞和成纤维细胞对植入装置材料的反应。使用光学和扫描电子显微镜检查暴露于 10 × 3 × 1 mm 镍、钛或镍钛合金片后支气管上皮细胞和肺成纤维细胞的粘附和增殖。评估促炎细胞因子 mRNA 表达和释放、信号激酶活性和细胞内自由基产生。镍钛诺以及较小程度的镍和钛表面支持肺上皮细胞的附着和生长。镍钛合金会引起激酶活性快速而显着的改变。直接暴露于镍或钛的细胞会产生自由基，但暴露于镍钛诺的细胞则不会。肺上皮细胞和成纤维细胞的反应取决于它们所接触的金属类型。镍钛诺会诱导细胞表面生长并诱导激酶活性，而肺上皮细胞暴露于镍和钛会诱导自由基产生，但镍钛诺不会。

图形概要