Pulmonary Surfactant Protein A Enhances the Host-defense Mechanism of Rat Alveolar Macrophages

Abstract

Abstract The effects of surfactant, surfactant lipids, and surfactant protein A (SP-A) on the surface phagocytosis of [3H]thymidine-labeled Staphylococcus aureus (SAE) by rat alveolar macrophages were studied. Alveolar macrophages only ingest SAE when the bacteria are opsonized with rat serum prior to incubation with alveolar macrophages. Preincubation or “opsonization” of the bacteria with surfactant did not result in phagocytosis by the macrophages. However, preincubation of the macrophages with surfactant increased the phagocytosis of rat serum-opsonized bacteria by approximately 70% when compared to the control macrophages. The factor present in surfactant causing the stimulation of the phagocytosis is probably SP-A. Preincubation of macrophages with human SP-A enhanced the phagocytosis to the same extent as whole surfactant, whereas preincubation with surfactant lipids had no effect on the phagocytosis. The SP-A-induced enhancement of the phagocytosis is time, temperature, and concentration dependent. Phagocytosis of opsonized SAE by alveolar macrophages was maximal after 15 min of incubation and at an SP-A concentration of 1 µg/ml. No phagocytosis occurred at 0° C. In addition, whole surfactant and SP-A induce a lucigenin-dependent chemiluminescence response in alveolar macrophages. The chemiluminescence response is initiated after 15 min of incubation and reaches a maximum after 30 min. The concentration of SP-A needed for an optimal response is in the same order of magnitude as the concentration needed for maximal enhancement of the phagocytosis of SAE by alveolar macrophages. The chemiluminescence response of alveolar macrophages incubated with SP-A and SAE together equals the sum of the responses of alveolar macrophages incubated with SP-A and SAE separately. This may indicate that SP-A and SAE act cooperatively in the generation of a chemiluminescence response by alveolar macrophages. The SP-A-induced response appears to be specific for alveolar macrophages, as peritoneal macrophages, polymorphonuclear leukocytes, and monocytes cannot be elicited by SP-A. This study demonstrates that SP-A potentiates the antibacterial functions of alveolar macrophages.