Pulmonary tissue and cigarette smoke: 1. Cellular response to hydrocortisone

Hydrocortisone acetate (HCA) administration significantly reduces the population of pulmonary macrophages and blood leukocytes in control, sham-treated, and smoke-exposed C57BL 6J mice. This treatment impedes markedly the influx of macrophages from bone marrow into the lungs. The small number of new phagocytes noted in lungs following HCA treatment appears to arise by proliferation of in situ pulmonary macrophages. Mortality rate of sham-treated and smoke-exposed mice was approximately twice that of control animals following HCA treatment. While severe pulmonary disorders were noted in lungs of HCA-treated, smoke-exposed animals, considerably milder abnormalities were seen in lungs of sham-treated mice. The data reported indicate that physical stress generated by manipulation during sham and smoke treatment, exposure to cigarette smoke, and reduction of pulmonary macrophages and leukocyte populations by HCA administration are factors which adversely affect pulmonary integrity and survival time of the animals.