Steady-state effects of vitronectin and fibronectin on the binding, uptake, and degradation of Pneumocystis carinii in rat alveolar macrophages.
Pneumocystis carinii pneumonia remains a serious complication of immunodeficiency. Vitronectin (VN) and fibronectin (FN) accumulate in the lung during P. carinii infection and bind to the organism, thereby enhancing macrophage release of TNF alpha. It is not known whether VN and FN also regulate uptake and degradation of P. carinii by macrophage when present in concentrations similar to those in the lung during pneumonia. To address this, macrophages were cultured with 35S-radiolabeled P. carinii and organism binding, phagocytosis, and degradation determined in media alone (control), or in the presence of VN or FN (100 micrograms/ml each). Soluble VN and FN, in concentrations similar to those in the host, did not significantly affect binding uptake or degradation of P. carinii by alveolar macrophages. Thus, although VN and FN enhance macrophage activation during P. carinii pneumonia, phagocytosis of the organism is not increased by these host glycoproteins under steady-state conditions.