EFFECT OF CORTICOSTEROIDS ON IL1-BETA AND TNF-ALPHA RELEASE BY ALVEOLAR MACROPHAGES FROM PATIENTS WITH AIDS AND PNEUMOCYSTIS-CARINII PNEUMONIA

The mechanisms by which corticosteroids (CCs) improve the outcome of AIDS patients with severe Pneumocystis carinii pneumonia (PCP) are unclear. We studied IL1beta and TNFalpha release from alveolar macrophages (AMs) of patients receiving CCs for the treatment of PCP and also the effect of in vitro hydrocortisone on this release. Cytokine release from AMs of AIDS patients with pulmonary complications not receiving CCs (group 1) was compared with that from AM of those receiving CCs for PCP (group 2). The AMs of E[IV-negative normal subjects (group 3) served as controls. All participants were nonsmokers or exsmokers. We found that lipopolysaccharide-stimulated AM from group 2 released significantly less interleukin-1 beta (IL1beta) and tumor necrosis factor alpha (TNFalpha) than AM from group 1 and was similar to that from group 3. There was a significant positive correlation between the amount of TNFalpha and IL1beta released. The presence of HC in the culture medium reduced in vitro IL1beta and TNFalpha release from stimulated AM of the three groups. Thus, stimulated AMs from AIDS patients who receive CCs for treatment of PCP release significantly less EL1beta and TNFalpha than AM from patients not receiving CCs. These findings suggest a mechanism by which CCs improve the outcome of AIDS patients with PCP.