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Articles in PresS, published online ahead of print September 28, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00120.2001
Submitted on March 29, 2001
Accepted on September 5, 2001
Alters Surfactant Lipid Metabolism
1 Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: james-carroll{at}uiowa.edu.
TNF- is a major cytokine implicated in inducing acute and chronic lung injury, conditions associated with surfactant phosphatidylcholine (PtdCho) deficiency. Acutely, TNF- decreases PtdCho synthesis but stimulates surfactant secretion. To investigate chronic effects of TNF-, we investigated PtdCho metabolism in a murine transgenic model exhibiting lung-specific TNF- overexpression. Compared to controls, TNF transgenic mice exhibited a discordant pattern of PtdCho metabolism, with a decrease in PtdCho and disaturated PtdCho (DSPtdCho) content in the lung, but increased levels in alveolar lavage. Transgenics had lower activities and increased immunoreactive levels of cytidylyltransferase (CCT), a key PtdCho biosynthetic enzyme. Ceramide, a CCT inhibitor, was elevated, and linoleic acid, a CCT activator, was decreased in transgenics. Radiolabeling studies revealed that alveolar reuptake of DSPtdCho was significantly decreased in transgenic mice. These observations suggest that chronic expression of TNF- results in a complex pattern of PtdCho metabolism where elevated lavage PtdCho may originate from alveolar inflammatory cells, decreased surfactant reuptake, or altered surfactant secretion. Reduced parenchymal PtdCho synthesis appears to be attributed to CCT enzyme that is physiologically inactivated by ceramide or by diminished availability of activating lipids.
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