Rola-Pleszczynski M, Gouin S, Bégin R
Inflammation. 1984 Mar;8(1):53-62. doi: 10.1007/BF00918353.
In a recently developed sheep model of progressive low-dose pulmonary exposure to asbestos, initial alveolar lymphocyte and macrophage activation was followed by pulmonary neutrophilia in higher-dose exposed animals. This was observed after 18 months of exposure to intratracheal instillations of asbestos fibers and coincided with progressive alveolitis and decreased lung compliance. Alveolar macrophages from those animals were found to produce a chemotactic factor which attracted in vitro peripheral blood neutrophils. It attracted neutrophils more efficiently from higher-exposure than lower-exposure animals. Supernatants of control macrophages exposed to asbestos in vitro were also chemotactic for PMN. Similarly, bronchoalveolar lavage fluids from the animals showed chemotactic activity for peripheral blood neutrophils. It is suggested that chronic exposure to asbestos activates alveolar macrophages to produce chemotactic factors which in turn attract neutrophils from the vascular compartment and may thus contribute to the inflammatory process in asbestosis.
在最近建立的绵羊渐进性低剂量肺部暴露于石棉的模型中，最初肺泡淋巴细胞和巨噬细胞被激活，随后高剂量暴露动物出现肺部嗜中性粒细胞增多。这一现象在气管内注入石棉纤维18个月后被观察到，同时伴有进行性肺泡炎和肺顺应性降低。发现那些动物的肺泡巨噬细胞产生一种趋化因子，该因子在体外吸引外周血中性粒细胞。与低暴露动物相比，它从高暴露动物中吸引中性粒细胞的效率更高。体外暴露于石棉的对照巨噬细胞的上清液对PMN也有趋化作用。同样，这些动物的支气管肺泡灌洗液对外周血中性粒细胞也表现出趋化活性。有人提出，长期暴露于石棉会激活肺泡巨噬细胞产生趋化因子，进而从血管腔吸引中性粒细胞，从而可能导致石棉沉着病的炎症过程。
