Rimland D, Hand W L
J Lab Clin Med. 1980 Jun;95(6):918-26.
Several defects in host defense mechanisms of chronic alcoholics have been described, but the effect of ethanol on the alveolar macrophage has not been defined. Monolayers of rabbit alveolar macrophages established on plastic culture dishes were exposed to various agents to evaluate the maintenance of adherence. Ethanol produces a rapid onset loss of adherence in this system. The loss of adherence is (1) dose-dependent, (2) transient despite the continued presence of ethanol, and (3) due to a change in the macrophage. Similar rapid-onset, transient loss of adherence is produced by osmolar agents, inducers of cAMP, and colchicine. Phagocytosis of latex particles by rabbit alveolar macrophages in suspension is also transiently decreased by ethanol. These results suggest that inhibition of alveolar macrophage adherence and phagocytosis may be mediated by one or a combination of three mechanisms: osmolar forces altering the cell membrane, changes in cyctic nucleotide concentrations, or disruption of microtubules. Ethanol may act through some combination of these mechanisms to produce functional abnormalities of alveolar macrophages.
