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Abstract
NORMAL antibacterial activity in the lung is largely dependent on alveolar macrophage function1. Products of antigen-stimulated, sensitised lymphocytes can activate alveolar macrophages, which then exhibit greater adherence, phagocytosis and nonspecific bactericidal capacity than normal2. Although the molecular basis of this activation is unknown, influx or intracellular redistribution of divalent cations (Ca2+ and Mg2+) has been implicated in other cell types3–10. We have therefore examined the effect on alveolar macrophage function of exposure to the ionophore A23187, which selectively binds divalent cations at neutral pH and passively transfers them across biological membranes11,12.
Published Version
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