Background: Surfactant synthesis and secretion has been shown to be impaired in type II cells from diseased lungs. The mechanism of surfactant lipid recycling, which is an important physiological process in surfactant treatment, was studied in type II cells isolated from injured lungs.
Methods: Different stages of lung injury were induced by exposing rats to 10 ppm nitrogen dioxide (NO2) for 3, 20, and 28 days. Type II cells were isolated from these lungs and recycling of 3H-DPPC labelled surfactant-like liposomes was studied in vitro.
Results: Uptake of liposomes (150 μg/ml) for 20 minutes in the absence and presence of surfactant protein-A (SP-A, 5 μg/ml) was higher in cells from NO2 injured lungs (63–78%) than in control cells. There was no difference in liposome uptake between the groups with NO2 exposure of different duration. After liposome uptake, most of the internalised label remained in the phosphatidylcholine (PC) fraction and increased with duration of exposure to NO2. After 20 minutes internalisation, cells were allowed to resecrete lipids for a further 20 minute period. In cells from controls and from all stages of lung injury, liposomes that had been internalised in the presence of SP-A were resecreted to a greater extent than those internalised without SP-A. However, cells from lungs exposed to NO2 resecreted less lipid than cells from control lungs. Again, there was no difference in resecretion between the groups with NO2 exposure of different duration.
Conclusion: Type II cells from injured lungs internalise more surfactant-like liposomes than cells from controls, suggesting a putative therapeutic significance to cope with limited alveolar surfactant pools in lung injury.
- surfactant system
- nitrogen dioxide
- type II pneumocytes
- bronchoalveolar lavage
- surfactant-like liposomes
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The study was supported by the BMBF Grant No. 01GC6901/5, Clinical Research group “Chronic Lung Injury”.
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