Abstract
The regulatory mechanism of degranulation of guinea pig peritoneal eosinophils was studied by determination of eosinophil peroxidase(EPO)release.β−Agonists, such as isoproterenol, salbutamol and fenoterol, effectively inhibited A23187−induced EPO release from guinea pig eosinophils.The inhibitory effects of β−agonists were attenuated by pretreatment with either propranolol, a non−selective β−antagonist, or ICI 118, 551, a selective β2−antagonist.Both theophylline and dibutyryl−cAMP(db−cAMP)also significantly inhibited A23187−induced EPO release.The inhibition of EPO release induced by db−cAMP was attenuated by pretreatment with KT5720, a protein kinase A inhibitor.In addition, calphostin C as well as cytochalasin D effectively inhibited A23187−induced EPO release.From the results of the present study, it was concluded that an increase in intracellular Ca2+ concentration may lead to exocytosis of eosinophil granules through activation of protein kinase C and microfilaments.β−Agonists and theophylline were effective in inhibiting degranulation of eosinophils by increasing intracellular cAMP level coupled with the activation of protein kinase A.
