[The role of pulmonary macrophages in the development of pulmonary fibrosis caused by asbestos].
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.
Lewczuk
E
E
Kliniki Chorób Wewnetrznych i Zawodowych, Akademii Medycznej we Wrocławiu.
Owczarek
H
H
Stanislawska
G
G
D000818:Animals; D001195:Asbestosis / Q000209:etiology*; D003094:Collagen / Q000096:biosynthesis; D006801:Humans; D016676:Macrophages, Alveolar / Q000502:physiology*; D010587:Phagocytosis / Q000502:physiology
D003094:Collagen
Udział makrofagów płucnych w procesie zwłóknienia płuc wywołanego pyłem azbestowym.