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on surfactant
metabolism
Department of Internal Medicine and the Department of Veterans Affairs Medical Center, University of Iowa College of Medicine, Iowa City, Iowa 52242
Tumor necrosis
factor-
(TNF-) has been shown to play an integral role in the
pathogenesis of the acute respiratory distress syndrome. This disorder
is characterized by a deficiency of alveolar surfactant, a
surface-active material that is composed of key hydrophobic proteins
and the major lipid disaturated phosphatidylcholine (DSPC). We
investigated how TNF- might alter DSPC content in rat lungs by
instilling the cytokine (2.5 µg) intratracheally for 10 min and then
assaying parameters of DSPC synthesis and degradation in alveolar type
II epithelial cells, which produce surfactant. Cells isolated from rats
given TNF- had 26% lower levels of phosphatidylcholine compared
with control. TNF- treatment also decreased the ability of these
cells to incorporate [3H]choline into DSPC by
45% compared with control isolates. There were no significant
differences in the levels of choline substrate or choline transport
between the groups. However, TNF- produced a 64% decrease in the
activity of cytidylyltransferase, the rate-regulatory enzyme required
for DSPC synthesis. TNF- administration in vivo also tended to
stimulate phospholipase A2 activity, but it did not alter
other parameters for DSPC degradation such as activities for
phosphatidylcholine-specific phospholipase C or phospholipase D. These
observations indicate that TNF- decreases the levels of surfactant
lipid by decreasing the activity of a key enzyme involved in surfactant
lipid synthesis. The results do not exclude stimulatory effects of the
cytokine on phosphatidylcholine breakdown.
alveolar type II epithelial cells; cytidylyltransferase respiratory
distress syndrome; tumor necrosis factor-
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