Endotoxin suppresses surfactant synthesis in cultured rat lung cells.
Pulmonary complications secondary to postburn sepsis are a major cause of death in burned patients. Using an in vitro organotypic culture system, we examined the effect of E. coli endotoxin (LPS) on lung cell surfactant synthesis. Our results showed that E. coli endotoxin (1.0, 2.5, 10 micrograms LPS/ml) was capable of suppressing the incorporation of 3H-choline into de novo synthesized surfactant, lamellar bodies (LB), and common myelin figures (CMF) at 50%, 68%, and 64%, respectively. In a similar study, we were able to show that LPS also inhibited 3H-palmitate incorporation by cultured lung cells. LPS-induced suppression of surfactant synthesis was reversed by hydrocortisone. Our results suggest that LPS may play a significant role in reducing surfactant synthesis by rat lung cells, and thus contribute to the pathogenesis of sepsis-related respiratory distress syndrome (RDS) in burn injury.
Li
J J
JJ
Shriners Burns Institute, Massachusetts General Hospital, Boston.
Sanders
R L
RL
McAdam
K P
KP
Gelfand
J A
JA
Burke
J F
JF
D000818:Animals; D002478:Cells, Cultured; D002794:Choline / Q000378:metabolism; D004247:DNA / Q000032:analysis / Q000187:drug effects; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D006854:Hydrocortisone / Q000494:pharmacology; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D011663:Pulmonary Surfactants / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D051381:Rats; D013050:Spectrometry, Fluorescence; D014316:Tritium
D004731:Endotoxins; D011663:Pulmonary Surfactants; D014316:Tritium; D004247:DNA; D002794:Choline; D006854:Hydrocortisone