Stimulation of Neutrophil Chemiluminescence by Alveolar Macrophages from Patients Exposed to Asbestos

Abstract

The effects of exposure to asbestos on the induction of pulmonary fibrosis, bronchial carcinoma and pleural mesothelioma have been extensively investigated (Craighead and Mossman 1982), but the mechanisms by which asbestos fibers induce pulmonary inflammation are not completely understood. Physical and chemical characteristics of the fibers (Kaw, Tilkes and Beck 1982), as well as their direct and indirect interaction with lung cells, seem to be implicated in the inflammatory process. Asbestos fibers can induce the release of several lysosomal enzymes and neutral proteinases from leukocytes (Davies and Allison 1976; Miller and Harrington 1972), contributing to pulmonary inflammation. In addition we have recently described, in later stages of experimental asbestosis, a marked increase in PMN influx into the lungs as well as a peripheral blood neutrophilia (Bégin et al. 1981; Bégin et al. 1983 a; Bégin et al. 1983 b; Rola-Pleszczynski, Gouin and Begin 1984). Polymorphonuclear leukocytes can contribute to pathogenesis of lung disease by releasing toxic oxygen by-products. We have recently shown that asbestos fibers can directly enhance PMN metabolic activity, as measured by the oxidative burst detected as chemiluminescence (CL) (Rola-Pleszczynski, Rivest and Bérardi 1984). Upon contact with or ingestion of particulate matter, oxidative species such as superoxide anion O₂ (Babior 1978; Badwey and Karnowsky 1980), hydroxyl radical (OH^.) (Green et al. 1979; Tauber and Babior 1977), hydrogen peroxyde H₂O₂, and oxygen singlet ¹O₂ ^. are generated by the activation of the NADPH oxidase and myeloperoxidase systems (De Chatelet and Long 1982) and also via the arachidonic acid pathway (Yashimoto et al. 1982; Cheung et al. 1983).