4-4-difluoro-4-bora-3a-4a-diaza-s-indacene and Pneumonia

Pulmonary surfactant reduces surface tension at the lung air-liquid interface and defends the host against infection. Several lines of evidence show that surfactant levels are altered in animal models and patients with inflammatory or infectious lung diseases. We tested the hypothesis that cells responding to lung injury alter surfactant levels through increased phospholipid clearance. Acute lung injury was induced by intratracheal administration of lipopolysaccharide (LPS; Escherichia coli 026:B6) into rats. LPS exposure resulted in a 12-fold increase in the number of cells isolated by lavage, the majority of which were neutrophils. Isolated macrophages and neutrophils from LPS-treated lungs internalized and degraded lipids in vitro, and LPS injury stimulated uptake by macrophages twofold. We estimate that lipid clearance by lavage cells in LPS-treated lungs could be enhanced 6- to 13-fold with both activated macrophages and increased numbers of neutrophils contributing to the process. These data show that the increased number of cells in the alveolar space after acute lung injury may lead to alterations in surfactant pools via enhanced clearance and degradation of lipids.

Topics: Acute Disease; Animals; Boron Compounds; Bronchoalveolar Lavage Fluid; Fluorescent Dyes; In Vitro Techniques; Lipopolysaccharides; Macrophages, Alveolar; Male; Neutrophils; Phosphorylcholine; Pneumonia; Proteolipids; Pulmonary Alveoli; Pulmonary Surfactant-Associated Proteins; Pulmonary Surfactants; Rats; Rats, Sprague-Dawley; Temperature