Role of alveolar macrophages in asbestosis: modulation of neutrophil migration to the lung after acute asbestos exposure.

Abstract

After intratracheal injection of short chrysotile asbestos fibers in guinea pigs, an intense neutrophil alveolitis was observed within 3 days. Evaluation by bronchoalveolar lavage of the inflammatory and immune effector cells producing the alveolitis by 3 days showed an increased proportion of polymorphonuclear leukocytes, which comprised 21 .+-. 3% of the total leukocytes compared with 9 .+-. 2% for the controls [P < 0.05), persisting for at least 6 wk (after which time the polymorphonuclear leukocytes comprised 28 .+-. 2% compared with 7 .+-. 1% for the controls: (P < 0.05). Asbestos fibers may cause polymorphonuclear leukocytes to be attracted to the alveolar structures by induced release of neutrophil chemotactic factor by alveolar macrophages. When exposed in vitro to short or intermediate chrysotile fibers or amosite or crocidolite fibers, guinea pig alveolar macrophages released appreciable amounts of neutrophil chemotactic factor. The release of this chemotactic factor was augmented when the asbestos fibers had been previously exposed to normal serum. The chmotactic factor was lipid soluble, and was similar to the neutrophil chemotactic factor spontaneously released by alveolar macrophages recovered from guinea pigs exposed in vivo to short chrysotile fibers. Alveolar macrophages may play an improtant part in the early stages of asbestosis by modulating the migration of neutrophils to the lung.