The interaction of chrysotile asbestos with alveolar macrophages in vitro is known to stimulate cellular superoxide anion production. However, it is likely that particulates in the respiratory tract are present together with components of the pulmonary surfactant, and it is not known how these components may alter the bioactivity of the particulate. We now show that guinea pig immunoglobulin G, a surfactant protein, causes a significant, dose-dependent enhancement of superoxide anion production by nonadherent guinea pig alveolar macrophages in response to chrysotile asbestos. This enhancement could not be mimicked by other particulates or proteins, including IgG fragments, implying that the interaction between IgG, cell, and chrysotile is relatively specific. The enhancing effect of IgG in solution could be reproduced by pretreating the chrysotile asbestos with IgG. The fact that IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production, in turn, leads to a proposal for a molecular mechanism by which asbestos may stimulate the guinea pig macrophage, namely, by crosslinking cell-surface immunoglobulin Fc receptors. In view of the submicromolar concentrations at which IgG was effective in enhancing macrophage stimulation by chrysotile asbestos in vitro, these results also suggest that IgG adsorption may play a role in the progression of asbestos-induced pulmonary fibrosis.
|Number of pages
|American Journal of Respiratory Cell and Molecular Biology
|Published - Oct 1989