Publication | Open Access
Activation of human basophils by staphylococcal protein A. I. The role of cyclic AMP, arachidonic acid metabolites, microtubules and microfilaments.
29
Citations
27
References
1982
Year
Signal TransductionAllergyBiochemistryHuman BasophilsEnhance Histamine ReleaseStaphylococcal Protein A.MedicineBacteriologyMechanism Of ActionCyclic AmpMicrobiologyMolecular MicrobiologyHistamine SecretionPharmacologyHistamine ReleaseDrug DiscoveryPhagocyteDrug Resistance
Protein A from Staphylococcus aureus (Staph A) induces histamine secretion from human basophil leucocytes in the concentration range 10(-4) - 10 micrograms/ml. This reaction has great similarities to that of antigen or anti-IgE-induced release. It is characterized by a two stage reaction, requires extracellular calcium and is optimal at 37 degrees C. The rate of release is similar to that of IgE-mediated reactions. Histamine release induced by Staph A is inhibited by metabolic inhibitors, drugs which increase intracellular cyclic AMP levels, inhibitors of lipoxygenase pathways and a phospholipase A2 inhibitor. D2O and cytochalasin B which affect microtubules and microfilaments respectively, enhance histamine release induced by Staph A. These results suggest that Staph A-induced release is modulated by intracellular cyclic AMP, arachidonic acid metabolites, requires energy and is enhanced by the disruption of microfilaments and stabilization of microtubules.
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