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Regulation of LPS‐stimulated IL‐10 secretion by PKC in macrophages.
Author(s) -
Fronhofer Van,
Loegering Daniel J
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a702
Subject(s) - secretion , protein kinase c , rottlerin , cytokine , microbiology and biotechnology , chemistry , macrophage , signal transduction , biology , endocrinology , immunology , biochemistry , in vitro
IL‐10 is a potent anti‐inflammatory cytokine produced by a variety of leukocytes including macrophages. It is important to understand the regulation of IL‐10 because of its ability to influence the immune response and suppress inflammation. Macrophages stimulated with LPS secrete small amounts of IL‐10. However, when combined with FcγR ligation LPS induces the production of large amounts of IL‐10 by macrophages. The signaling pathways responsible for LPS‐stimulated IL‐10 and the positive effect of the FcγR on LPS‐stimulated IL‐10 production are not well characterized. PKC is activated by LPS and that activation is altered by FcγR ligation in macrophages. This study evaluated the role of PKC in LPS‐stimulated IL‐10 secretion and the effect of FcγR ligation on LPS‐stimulated IL‐10 secretion by mouse peritoneal macrophages. Inhibition of PKC with Gö6976 or Rottlerin decreased LPS‐stimulated IL‐10 secretion and rescued the effects of FcγR ligation. However, depletion of PKC‐α and PKC‐ε isoforms with antisense DNA oligonucleotides augmented LPS‐stimulated IL‐10 secretion. Depletion of PKC‐δ with antisense had no effect on LPS‐stimulated IL‐10 secretion and did not alter the influence of FcγR ligation on LPS‐stimulated IL‐10 secretion. Thus PKC‐δ appears to have no role in the regulation of LPS‐stimulated IL‐10 secretion by mouse macrophages where as PKC‐α and ‐ε may have a negative influence on LPS‐stimulated IL‐10 secretion. This study was supported by the American Heart Association Grant 50893T.