TY - JOUR
T1 - Activation of human basophils by staphylococcal protein A. I. The role of cyclic AMP, arachidonic acid metabolites, microtubules and microfilaments
AU - Marone, G.
AU - Poto, S.
AU - Petracca, R.
AU - Triggiani, M.
AU - de Lutio di Castelguidone, E.
AU - Condorelli, M.
PY - 1982
Y1 - 1982
N2 - Protein A from Staphylococcus aureus (Staph a) induces histamine secretion from human basophil leucocytes in the concentration range 10 -4-10 μg/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°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 A 2 inhibitor, D 2O 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 microgifaments and stabilization of microtubules.
AB - Protein A from Staphylococcus aureus (Staph a) induces histamine secretion from human basophil leucocytes in the concentration range 10 -4-10 μg/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°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 A 2 inhibitor, D 2O 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 microgifaments and stabilization of microtubules.
UR - http://www.scopus.com/inward/record.url?scp=0020401320&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0020401320&partnerID=8YFLogxK
M3 - Article
C2 - 6299635
AN - SCOPUS:0020401320
SN - 0009-9104
VL - 50
SP - 661
EP - 668
JO - Clinical and Experimental Immunology
JF - Clinical and Experimental Immunology
IS - 3
ER -