Discrete pathways for arachidonic acid release from tannin versus β-glucan-stimulated rabbit alveolar macrophages

M. T. Kennedy*, P. J. Bates, C. L. Wheatley, M. S. Rohrbach

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Previously, we observed both tannin and β-glucan to be agonists for arachidonic acid (AA) release from rabbit alveolar macrophages. Although tannin inhibited reincorporation of exogenous AA, β-glucan had no apparent effect, suggesting separate signal transduction pathways leading to elevated AA levels. In this study alveolar macrophages were pretreated with the tyrosine phosphatase inhibitor sodium orthovanadate then stimulated with either condensed tannin or β-glucan. Vanadate exerted opposing effects on AA release. Furthermore, vanadate reversed the ability of tannin to inhibit reacylation. Additional studies using the phospholipase A probe bis-BODIPY-C11-PC indicated that although the known phospholipase A2 activators, calcium ionophore A23187, insoluble immune complexes, and β-glucan, generated an increase in fluorescence consistent with phospholipase A activation, tannin had no effect. These findings suggest the increase in free AA resulting from stimulation of macrophages by either tannin or β-glucan is produced via two different mechanisms.

Original languageEnglish (US)
Pages (from-to)241-248
Number of pages8
JournalJournal of Leukocyte Biology
Volume58
Issue number2
DOIs
StatePublished - 1995

Keywords

  • Lands cycle
  • PLA
  • Reacylation
  • Tyrosine phosphorylation
  • Vanadate

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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