The effects of cortisone therapy on lung macrophage host defense function and glucose metabolism

The administration of high-dose glucocorticoid therapy in the treatment of lung inflammatory and immune diseases often results in an increased susceptibility to pulmonary infections. The effects of cortisone therapy on the phagocytic function and glucose metabolism of alveolar macrophages (AM) were evaluated in guinea pigs treated for 7 days with 100 mg/kg of cortisone acetate. AM were harvested 24 hours following the final daily drug treatment by lung lavage techniques. Cortisone treatment produced a profound leukocytosis, lymphocytopenia, and monocytopenia in the peripheral blood while decreasing by greater than 40% the number of AM obtainable by lung washings. Macrophage phagocytosis, as assessed by the in vitro uptake of radiolabeled heat-killed Pseudomonas aeruginosa by monolayers of lung macrophages, was depressed in AM harvested from cortisone-treated animals. In addition, cortisone therapy also inhibited the stimulation in glucose oxidation normally associated with macrophage phagocytosis as well as depressing the membrane transport of 2-deoxyglucose. These results demonstrate that high-dose cortisone therapy can impair both functional and metabolic activities of the phagocytic defense mechanism of the lower respiratory tract.