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Am J Physiol Lung Cell Mol Physiol 281: L268-L277, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 1, L268-L277, July 2001

Enhanced clearance of surfactant protein D during LPS-induced acute inflammation in rat lung

Joel F. Herbein and Jo Rae Wright

Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710

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.

type II cells; neutrophils; macrophages; surfactant recycling; surfactant protein A; lipopolysaccharide


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