Control function of protein kinase C isozymes on leukotriene generation from human basophils?
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Arachidonic acid metabolites generated from activated basophils and/or mast cells mediate different types of cutaneous inflammatory reactions. To clarify the mechanisms of leukotriene C4 (LTC4) production from human basophils, cells were purified from the peripheral blood by negative selection with immunobeads. The protein kinase C (PKC) activators 12-O-tetradecanoyl-phorbol-13-acetate, phorbol-12,13-dibutyrate and phorbol-12,13-didecanoate did not induce a significant LTC4 generation from human basophilsin vitro, indicating that phorbol-ester-sensitive PKC isozymes are not involved in the mechanisms of arachidonic acid metabolism in these cells. However, selective PKC inhibitors (Ro 31-7549, ilmofosine, GF109203X, and calphostin C) potentiated the IgE-mediated LTC4 production in a dose-dependent fashion. We therefore suggest that PKC isozymes which are influenced by these inhibitors modulate the degree of LTC4 release after stimulation with anti-IgE antibodies.
KeywordsMast Cell Arachidonic Acid Acid Metabolite Arachidonic Acid Metabolism Arachidonic Acid Metabolite
protein kinase C
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