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Am J Physiol Lung Cell Mol Physiol 277: L777-L786, 1999;
1040-0605/99 $5.00
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Vol. 277, Issue 4, L777-L786, October 1999

Surfactant protein A enhances alveolar macrophage phagocytosis of a live, mucoid strain of P. aeruginosa

William I. Mariencheck1, Jordan Savov2, Qun Dong3, Michael James Tino3, and Jo Rae Wright1,3

Departments of 1 Medicine and 3 Cell Biology and 2 Durham Veterans Affairs Medical Center Research Service, Duke University Medical Center, Durham, North Carolina 27710

In this study, we investigate the interaction between surfactant protein A (SP-A) and a live, mucoid strain of Pseudomonas aeruginosa and identify a mechanism of clearance of this organism by alveolar macrophages. 125I-labeled SP-A bound live, but not heat-killed, P. aeruginosa organisms in a concentration-dependent manner. Unlabeled SP-A bound live bacteria, protein isolated from whole organisms, and specific proteins of the P. aeruginosa outer membrane. The binding of SP-A to P. aeruginosa and outer membrane components was inhibited by either EDTA or mannose. Phagocytosis assays with fluorescent microscopy demonstrated that the percentage of macrophages with internalized FITC-labeled P. aeruginosa was increased 1.8-fold (19 vs. 35%) by pretreating the live bacteria with SP-A. This finding was confirmed by direct visualization of ingested bacteria by electron microscopy. Adhering macrophages to SP-A-coated surfaces attenuated the increased uptake of P. aeruginosa pretreated with SP-A, suggesting that SP-A acts as an opsonin to stimulate macrophage phagocytosis of this strain of P. aeruginosa.

Pseudomonas aeruginosa; lung infection; innate immunity; cystic fibrosis


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