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Discrete pathways for arachidonic acid release from tannin versus β‐glucan‐stimulated rabbit alveolar macrophages
Author(s) -
Kennedy Michael T.,
Bates Philip J.,
Wheatley Christine L.,
Rohrbach Michael S.
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.58.2.241
Subject(s) - arachidonic acid , biochemistry , glucan , phospholipase , tannin , sodium orthovanadate , phospholipase a2 , vanadate , phospholipase a , biology , phospholipase c , phosphatase , signal transduction , enzyme , food science
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‐C 11 ‐i‐PC indicated that although the known phospholipase A 2 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. J. Leukoc. Biol. 58: 241–248; 1995.