Lewczuk E, Owczarek H, Stanislawska G
Kliniki Chorób Wewnetrznych i Zawodowych, Akademii Medycznej we Wrocławiu.
Med Pr. 1994;45(4):351-7.
The role of alveolar and interstitial macrophages in asbestos-induced pulmonary fibrosis is discussed. Asbestosis is thought to result from a series of cellular interaction involving the pulmonary macrophages and lung fibroblasts. Inhaled asbestos fibres activate serum complement-dependent chemoattractant for macrophages which accumulate at alveolar duct bifurcations playing a central role in phagocytosis fibers and forming early pulmonary lesions. After phagocytic stimulation macrophages release various chemotactic factors for neutrophils and other inflammatory cells including TNF, neutrophil chemotactic factor and many proinflammatory mediators such as prostaglandins, leukotrienes, thromboxane. Apart from that, macrophages produce free radical oxygen and release lysosome enzymes which may cause lung tissue injury. There is also concomitant accumulation of fibroblasts proliferating in response to macrophages-derived growth factors, interleukin-1 and fibronectin. As a result of those processes collagen production increase and pulmonary fibrosis develops.
本文讨论了肺泡巨噬细胞和间质巨噬细胞在石棉诱导的肺纤维化中的作用。石棉肺被认为是由一系列涉及肺巨噬细胞和肺成纤维细胞的细胞相互作用所导致的。吸入的石棉纤维激活血清补体依赖性巨噬细胞趋化因子，这些巨噬细胞聚集在肺泡管分支处，在吞噬纤维和形成早期肺部病变中起核心作用。吞噬刺激后，巨噬细胞释放多种针对中性粒细胞和其他炎症细胞的趋化因子，包括肿瘤坏死因子、中性粒细胞趋化因子以及许多促炎介质，如前列腺素、白三烯、血栓素。除此之外，巨噬细胞产生自由基氧并释放溶酶体酶，这可能会导致肺组织损伤。同时，成纤维细胞也会因巨噬细胞衍生的生长因子、白细胞介素-1和纤连蛋白而增殖并积聚。这些过程导致胶原蛋白生成增加，进而发展为肺纤维化。
