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Modulation of human microglial cell superoxide production by cytokines
Author(s) -
Chao Chun C.,
Hu Shuxian,
Peterson Phillip K.
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.58.1.65
Subject(s) - microglia , superoxide , tumor necrosis factor alpha , biology , reactive oxygen species , microbiology and biotechnology , priming (agriculture) , stimulation , cytokine , phorbol , interleukin , signal transduction , protein kinase c , neuroglia , interferon gamma , interferon , immunology , inflammation , biochemistry , endocrinology , central nervous system , botany , germination , enzyme
Reactive oxygen intermediates (e.g., superoxide [O 2 ‐ ]) generated by microglia may play a role in host defense and injury within the central nervous system. We investigated the effect of cytokines on human microglial cell O 2 ‐ production on stimulation with phorbol myristate acetate. Priming of microglial cell cultures with interferon‐γ or tumor necrosis factor‐α resulted in a dose‐ and time‐dependent enhancement of (O 2 ‐ production. The priming effects of these cytokines were mediated through a protein kinase C signal transduction pathway. In contrast, astrocytes did not generate detectable O 2 ‐ on phorbol myristate acetate stimulation. Treatment of microglia with transforming growth factor‐β, interleukin‐4, or interleukin‐10 suppressed in a dose‐dependent manner the priming effects of tumor necrosis factor‐α and interferon‐γ. The results of this study have implications for understanding the mechanisms by which cytokines and microglia contribute to processes of host defense and neurodegeneiration via generation of reactive oxygen intermediates. J. Leukoc. Biol. 58: 65–70; 1995.

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