Platelet-activating factor or a platelet-activating factor antagonist decreases tumor necrosis Factor-α in the plasma of mice treated with endotoxin

Kim M. Ferguson-Chanowitz, Andrew S. Katocs, Walter C. Pickett, Jeffrey B. Kaplan, Philip M. Sass, Arnold L. Oronsky, S. S. Kerwar

Research output: Contribution to journalArticle

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 (TNFα) 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 TNFα levels in LPS-treated mice. The decrease in plasma TNFα induced by L-PAF or alprazolam was partly reversed by indomethacin. Despite a decrease in plasma TNFα, L-PAF or alprazolam caused an increase in the amount of TNFα mRNA present in the kidneys and the livers of LPS-treated mice, suggesting that a posttranscriptional event leading to the synthesis or release of TNFα was inhibited by these agents.

Original languageEnglish (US)
Pages (from-to)1081-1086
Number of pages6
JournalJournal of Infectious Diseases
Volume162
Issue number5
DOIs
StatePublished - Nov 1990

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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    Ferguson-Chanowitz, K. M., Katocs, A. S., Pickett, W. C., Kaplan, J. B., Sass, P. M., Oronsky, A. L., & Kerwar, S. S. (1990). Platelet-activating factor or a platelet-activating factor antagonist decreases tumor necrosis Factor-α in the plasma of mice treated with endotoxin. Journal of Infectious Diseases, 162(5), 1081-1086. https://doi.org/10.1093/infdis/162.5.1081