One of the major host-defense functions of alveolar macrophages is the phagocytosis and clearance of inhaled particles deposited in the lower airways and alveolar spaces. Recent studies have indicated that the
condensed tannins present in cotton mill dust stimulate the secretion of
neutrophil chemotactic factor and
arachidonic acid from resident rabbit alveolar macrophages and that these responses may contribute to the acute pulmonary inflammatory reaction associated with
byssinosis. To characterize further the effect of
tannin on macrophage function, the ability of
tannin to modulate alveolar macrophage spreading and phagocytosis in vitro was examined.
Tannin caused a dose-dependent inhibition of alveolar macrophage spreading with nearly complete inhibition occurring at concentrations of 12.5 micrograms/ml. This inhibitory effect of
tannin was not reversed with removal of
tannin. Furthermore addition of
tannin to previously spread macrophages actively caused the macrophages to round up. Examination of the structure of alveolar macrophages exposed to
tannin by scanning and transmission electron microscopy revealed
blebs on the surface of the cells and the loss of most of the cellular organelle structure, as compared to control macrophages.
Tannin also modulated the ability of the alveolar macrophages to phagocytize unopsonized
latex microspheres. The effect of
tannin was biphasic. At the lowest concentration examined (3 micrograms/ml),
tannin significantly enhanced phagocytosis of the
latex microspheres. However, as the concentration was increased, phagocytosis decreased almost exponentially until at 50 micrograms/ml phagocytosis was significantly inhibited compared to control macrophages. These data indicate that
tannin present in inhaled cotton mill dust could significantly decrease the ability of resident alveolar macrophages to phagocytize and thereby clear inhaled dust particles. This inhibitory effect would increase the time that particles remain exposed in the lower airway and alveolar spaces and thereby increase the time that potentially toxic compounds in the dust have to exert their
biologic effect. This inhibition of macrophage function may therefore contribute to the pathogenesis of
byssinosis.