Abstract
BackgroundA decrease in pulmonary surfactant has been suggested to contribute to the lung dysfunction associated with pulmonary inflammation. A number of studies have implicated surfactant clearance as a possible mechanism for altered pool sizes. The objective of the current study was to specifically investigate the mechanisms of surfactant clearance in a rodent model of acute pulmonary inflammation.MethodsInflammation was induced by intrapulmonary instillation of lipopolysaccharide (LPS: 100 μg/kg). Lipid clearance was assessed at 18 and 72 hours post-LPS instillation by intratracheal administration of radiolabel surfactant-like liposomes 2 hours prior to isolation and analysis of inflammatory cells and type II cells.ResultsAt both 18 and 72 hours after LPS instillation there was significantly less radioactivity recovered in the lavage fluid compared to respective control groups (p < 0.05). At both time points, the number of cells recovered by lavage and their associated radioactivity was greater compared to control groups (p < 0.01). There was no difference in recovery of radioactivity by isolated type II cells or other cells obtained from enzymatic digestion of lung tissue.ConclusionThese results show that increased clearance of surfactant lipids in our model of acute pulmonary inflammation is primarily due to the inflammatory cells recruited to the airspace and not increased uptake by alveolar type II cells.
Highlights
A decrease in pulmonary surfactant has been suggested to contribute to the lung dysfunction associated with pulmonary inflammation
LPS-induced alterations: bronchoalveolar lavage fluid (BALF) cells and alveolar surfactant Table 1 reveals total alveolar cell numbers and differentials from the BALF of control and LPS groups killed at the 18- and 72-hour time points
Cell differentials from the two 18-hour groups revealed that the LPS group had primarily neutrophils in the BALF, whereas the cells recovered from the control group were predominantly macrophages
Summary
A decrease in pulmonary surfactant has been suggested to contribute to the lung dysfunction associated with pulmonary inflammation. Pulmonary surfactant is a phospholipid-protein complex that lines the inner surface of the lung and is essential for normal pulmonary function. The lipid component is primarily phospholipids with phosphatidylcholine (PC) being the most abundant, and the protein component comprised of four surfactant-associated proteins designated SP-A, SP-B, SP-C and SP-D [1]. The reduction of surface tension within the lung is a result of the interaction between surfactant phospholipids and the two hydrophobic surfactant proteins, SP-B and SP-C [1], while the two hydrophilic proteins, SP-A and SP-D, are members of a family of innate immune molecules called collectins [2]. Collectins opsonize bacteria and viruses and enhance their phagocytosis by macrophages and neutrophils [2]
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