Chronic, pulmonary fibrosis caused by the inhalation of asbestos has a very clear etiology, although its pathogenesis remains obscure. Macrophages are a key element in the response of the host to asbestos. Dust clearance from the alveoli is the function of the macrophages. Whereas these cells phagocytize short fibres and remove them from the respiratory pathways they cannot encompass and transport the longer fibres, which tend to be retained in the lumens of the bronchioles and the alveolar ducts (Craighead and Mossman, 1987). The appearance of asbestos bodies represents the endogenous reaction of the pulmonary defense mechanism to the inhaled needlelike asbestos. Asbestos bodies are inhaled asbestos fibres which have been coated with ferroprotein by macrophages (Morgan and Holmes, 1985). It is generally accepted that coating neutralises the pathogenic potential of the fibre. The coated fibres are less toxic to pulmonary alveolar macrophages (McLemaire et al., 1980). The fibres, the lengths of which exceed the diameter of the human alveolar macrophage (ca. 15 μm) are poorly cleared. As asbestos bodies are rarely formed on fibres less than 10 µm in length, the majority will be retained in the lungs indefinitely, unless broken into smaller fragments, which undergo phagocytosis and are cleared by macrophages (Timbrel, 1982).
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- The Significance of Asbestos Bodies and Occurrence of Macrophages in the Sputum of Asbestos-Exposed Workers
- Springer Berlin Heidelberg