Recent developments in studies investigating interactions of asbestos (1332214) with cells of the immune system were reviewed. The review summarized the pulmonary toxicity of asbestos and discussed recent studies investigating the effects of asbestos on nonspecific and specific immunity, and the role of iron (7439896) and reactive oxygen species in asbestos immunotoxicity. Occupational exposure to asbestos has been associated with increased risks for a range of pulmonary diseases and is considered to be an important cause of pulmonary malignancies, malignant mesothelioma and bronchiogenic carcinoma. The major disease associated with asbestos is asbestosis, which is an interstitial pulmonary fibrosis commonly thought to represent the terminal phase of a chronic inflammatory process. The inflammatory response along with peripheral immune changes following asbestos exposure has implicated the immune system in the pathogenesis of asbestos related disease. Studies investigating the effects of asbestos on nonspecific immunity have focused on the effects of exposure on natural killer (NK) cells, pulmonary macrophages, and pulmonary epithelial cells. Studies in laboratory animals have shown that asbestos impairs NK cell mediated cytotoxicity. Occupational asbestos exposure has been shown to decrease the number of circulating NK cells and to alter the number of local or interstitial NK cells in pulmonary tissues. Other studies have suggested that epithelial cells as well as macrophages and fibroblasts may be important effector cells in the immunopathogenesis of asbestos related diseases. Experimental studies and human observations have provided evidence that asbestos impairs specific mediated immunity and that these effects may be an important predisposing factor in asbestos induced fibrosis. Asbestos fibers as a result of the presence of iron on their surface may induce generation of reactive oxygen species which modulate intracellular redox states. This can contribute to the activation of transcription factors such as nuclear-factor-kappa-B and nuclear- factor-interleukin-6 which, in turn, stimulate inflammatory cytokines.
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