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A phagocytic challenge with IgG‐coated erythrocytes depresses macrophage respiratory burst and phagocytic function by different mechanisms
Author(s) -
Raley Michael J.,
Lennartz Michelle R.,
Loegering Daniel J.
Publication year - 1999
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.66.5.803
Subject(s) - respiratory burst , biology , phagocytosis , macrophage , immunology , respiratory system , function (biology) , microbiology and biotechnology , in vitro , biochemistry , anatomy
A phagocytic challenge with IgG‐coated erythrocytes (EIgG) previously has been shown to cause impaired macrophage respiratory burst capacity and FcγR‐mediated phagocytic function. Because both the respiratory burst and FcγR‐mediated phagocytosis are dependent on the release of arachidonate (AA), we evaluated the effects of impaired AA release on the depression of macrophage function caused by a phagocytic challenge. Challenge with EIgG caused a depression of A23187‐stimulated AA release that was associated with impaired phorbol myristate acetate (PMA)‐stimulated H 2 O 2 production and FcγR‐mediated phagocytic function. In contrast, challenge with IgG‐coated glass beads (BIgG) had no effect on either AA release or H 2 O 2 production but did depress phagocytic function. Exogenous AA prevented the depression of H 2 O 2 production but had no effect on phagocytic function. Phospholipase A 2 (PLA 2 ) activity was depressed under conditions where AA release was impaired. The depression of phagocytic function was correlated with a depression of both EIgG binding and FcγR expression. Thus, a phagocytic challenge with EIgG results in macrophage dysfunction by depressing PLA 2 activity and depleting FcγR. J. Leukoc. Biol. 66: 803–808; 1999.