Platelet-Activating Factor or a Platelet-Activating Factor Antagonist Decreases Tumor Necrosis Factor- in the Plasma of Mice Treated with Endotoxin

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Abstract
When L-platelet-activating factor (PAF) or alprazolam (a PAF antagonist) was administered to lipopolysaccharide (LPS)-treated mice, the level of plasma tumor necrosis factor (TNF.alpha.) determined by either ELISA or a cytotoxic assay using WEHI cells was significantly lowered. The inactive stereoisomer, D-PAF, was not effective in lowering plasma TNF.alpha. levels in LPS-treated mice. The decrease in plasma TNF.alpha. induced by L-PAF or alprazolam was partly reversed by indomethacin. Despite a decrease in plasma TNF-.alpha., L-PAF or alprazolam caused an increase in the amount of TNF.alpha. mRNA present in the kidneys and the livers of LPS-treated mice, suggesting that a posttranscriptional event leading to the synthesis or release of TNF.alpha. was inhibited by these agents.