Pulmonary macrophage accumulation and asbestos-induced lesions at sites of fiber deposition.
Inhaled chrysotile asbestos fibers are deposited at alveolar duct bifurcations and subsequently are phagocytized there by pulmonary macrophages. The characteristics of the rapid macrophage response at alveolar duct bifurcations following asbestos inhalation has been further evaluated. Significant numbers of pulmonary macrophages accumulated at sites of asbestos deposition within 48 h after a 1-h exposure, whereas duct surfaces of sham-exposed animals were essentially devoid of macrophages. The influx of macrophages was associated with a significantly increased bifurcation tissue area (p less than 0.025), and this alteration persisted for at least 1 month. Two thirds of the accumulated macrophages from alveolar duct bifurcations could be removed by bronchoalveolar lavage. Macrophages recovered by lavage had significant changes (p less than 0.01) in their morphology and in their phagocytic and chemotactic capacities. These cellular alterations could play a role in the pathogenesis of asbestos-related lung disease.
D000818:Animals; D001194:Asbestos / Q000032:analysis; D002465:Cell Movement; D002633:Chemotaxis; D008264:Macrophages / Q000032:analysis / Q000502:physiology / Q000648:ultrastructure*; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000648:ultrastructure*; D051381:Rats; D012119:Respiration; D007507:Therapeutic Irrigation
D001194:Asbestos