Pulmonary Surfactant Protein A Enhances the Host-defense Mechanism of Rat Alveolar Macrophages Freek van Iwaarden, Berris Welmers, Jan Verhoef, Henk P. Haagsman, and Lambert M. G. van Golde Laboratory of Veterinary Biochemistry, and Laboratory of Microbiology, University of Utrecht, Utrecht, The Netherlands

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 ofthe 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 SPA-induced enhancement of the phagocytosis is time, temperature, and concentration dependent. Phagocytosis of opsonized SAE by alveolar macrophages was maximal after IS min of incubation and at an SP-A concentration of I p.g/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.

Pulmonary surfactant is a complex of lipids, proteins, and carbohydrates that lines the alveolar surfaces of the lung. One of its major functions is to prevent lung collapse at endexpiration. In 1973, La Force and associates (1) reported enhanced killing of Staphylococcus aureus by alveolar macrophages in the presence of surfactant and postulated a role fur surfactant in the host-defense system of the lung. Since then, several investigators reported stimulating effects of surfactant and surfactant lipids on the phagocytosis (2, 3) and killing ofbacKey Words: alveolar macrophages, pulmonary surfactant, phagocytosis, chemiluminescence (rat lung) (Received in original form April 11, 1989 and in revised form August 11, 1989) Address correspondence to: Dr. F. van Iwaarden, Laboratory of Veterinary Biochemistry, P.O. Box 80.176, 3508 TO Utrecht, The Netherlands. Abbreviations: Staphylococcus aureus Evers, SAE; surfactant protein A, SP-A. Am. J. Respir. Cell Mol. BioI. Vol. 2. pp. 91-98, 1990

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Pulmonary surfactant protein A enhances the host-defense mechanism of rat alveolar macrophages.

The effects of surfactant, surfactant lipids, and surfactant protein A (SP-A) on the surface phagocytosis of [3H]thymidine-labeled Staphylococcus aure...
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