ACTIVATION OF HUMAN BASOPHILS BY STAPHYLOCOCCAL PROTEIN-A .1. THE ROLE OF CYCLIC-AMP, ARACHIDONIC-ACID METABOLITES, MICROTUBULES AND MICROFILAMENTS

Google Scholar
  • 1 January 1982
    • journal article
    • research article
    • Vol. 50  (3) , 661-668
Abstract
Protein A from Staphlococcus aureus (Staph A) induces histamine secretion from human basophil leukocytes in the concentration range 10-4-10 .mu.g/ml. This reaction has great similarities to that of antigen or anti-IgE-induced release. It is characterized by a 2 stage reaction, requires extracellular Ca and is optimal at 37.degree. C. The rate of release is similar to that of IgE-mediated reactions. Histamine release induced by Staph A is inhibited by metabolic inhibitors [2-deoxy-D-glucose, antimycin A] drugs which increase intracellular cAMP levels [dibutyryl cAMP, 3-isobutyl-1-methylxanthine, prostaglandin E2, dimaprit], inhibitors of lipoxygenase pathways [5,8,11,14-eicosatetraenoic acid, 5,8,11-eicosatriynoic acid] and a phospholipase A2 inhibitor [p-bromophenacyl bromide]. D2O and cytochalasin B which affect microtubules and microfilaments, respectively, enhance histamine release induced by Staph A. Evidently, staph A-induced release is modulated by intracellular cAMP, arachidonic acid metabolites, requires energy and is enhanced by the disruption of microfilaments and stabilization of microtubules.

This publication has 31 references indexed in Scilit: