Pulmonary surfactant participates in the regulation of alveolar compliance and lung host defense.
Surfactant homeostasis is regulated through a combination of synthesis, secretion, clearance, recycling, and degradation of
surfactant components. The extracellular pool size of
surfactant protein (
SP) D fluctuates significantly during acute
inflammation. We hypothesized that changes in
SP-D levels are due, in part, to altered clearance of
SP-D. Clearance pathways in rats were assessed with fluorescently labeled
SP-D that was instilled into control lungs or lungs that had been treated with
lipopolysaccharide (LPS) 16 h earlier.
SP-D clearance from lavage into lung tissue was time dependent from 5 min to 1 h and 1.7-fold greater in LPS-treated lungs than in control lungs. Analysis of cells isolated by enzymatic digestion of lung tissue revealed differences in the
SP-D-positive cell population between groups. LPS-treated lungs had 28.1-fold more
SP-D-positive tissue-associated neutrophils and 193.6-fold greater
SP-D association with those neutrophils compared with control lungs. These data suggest that clearance of
SP-D into lung tissue is increased during
inflammation and that tissue-associated neutrophils significantly contribute to this process.