Pneumocystis carinii‐induced activation of the respiratory burst in human monocytes and macrophages

SUMMARY Human monocytes and monocyte‐derived macrophages were studied for their ability to phagocytose Pneumocystis carinii and produce superoxide (O − 2 ) during the process. One × 10 6 freshly isolated monocytes. incubated with 0.1 – 3.75 × 10 6 P. carinii cysts, increased O − 2 production in a dose‐related way. Antibodies were essential for the process since opsonized, but not unopsonized, pneumocysts induced O − 2 production significantly above the response obtained by lung tissue from rats (10.7 and 4.9 versus 30 fmol/cell per 90 min). The difference between pneumocysts opsonized in untreated versus complement‐depleted serum was not significant (10.7 versus 12.6 fmol/cell per 90 min). Monocyte‐derived macrophages also activated the respiratory burst when stimulated with pneumocysts, and this effect could be significantly increased, from 4.2 to 8.8 fmol/cell per 90 min, when cells were primed with interferon‐gamma (IEN‐γ). Cells primed with IL‐3 also increased O 2 production, though to a lesser extent. In contrast, granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) had only a small effect on the respiratory burst in cells stimulated with P. carinii. Priming with IEN‐γ increased the rate of phagocytosis in macrophages. After incubation for 90 min or more, however, the percentage of cells with phagocytic vacuoles was only slightly higher in IFN‐γ‐primed cells. When examined by electron microscopy (EM), most vacuoles contained partially or totally degraded pneumocysts. In conclusion, we have demonstrated the ability of monocytes and monocyte‐derived macrophages to ingest and degrade pneumocysts. activating the respiratory burst during the process.