TY - JOUR
T1 - Heterologous desensitization of leukocytes
T2 - a possible mechanism of beta adrenergic blockade in atopic dermatitis
AU - Safko, Martin J.
AU - Chan, Sai Chung
AU - Cooper, Kevin D.
AU - Hanifin, Jon M.
N1 - Funding Information:
From the Departmenotf Dermatology, Sciences Center, Portland, Ore. This study was supported by grants 5 ROL AI15557-2 and T T32 AM07153-05 from the National Institutes of Health and by a grant from the Medical Research Foundation of Oregon. Received for publication Aug. 19, 1980. Accepted for publication June 10, 198 1. Reprint requests to: Jon M. Hanifin, Department of Dermatology, University of Oregon Health Sciences Center, Portland, OR 97201.
PY - 1981/9
Y1 - 1981/9
N2 - Studies of mononuclear leukocytes from patients with atopic dermatitis showed depressed cyclic AMP (cAMP) responses after exposure to isoproterenol, histamine, and prostaglandin E1. Because plasma and tissue histamine levels are elevated in atopic dermatitis, we questioned whether histamine or other mediators might be responsible for cAMP abnormalities. We found that exposure of normal cells to low (10-6M) concentrations of histamine, isoproterenol, or prostaglandin E desensitized the cells to subsequent stimulatory concentrations of any of the agonists. This heterologous desensitization occurred within 15 min and persisted for days, with gradual recovery of cAMP responses roughly paralleling those of cells from patients with atopic dermatitis. These findings provide a possible explanation for Szentivanyi's beta adrenergic blockade theory and the depressed leukocyte cAMP response to multiple agonists in atopy.
AB - Studies of mononuclear leukocytes from patients with atopic dermatitis showed depressed cyclic AMP (cAMP) responses after exposure to isoproterenol, histamine, and prostaglandin E1. Because plasma and tissue histamine levels are elevated in atopic dermatitis, we questioned whether histamine or other mediators might be responsible for cAMP abnormalities. We found that exposure of normal cells to low (10-6M) concentrations of histamine, isoproterenol, or prostaglandin E desensitized the cells to subsequent stimulatory concentrations of any of the agonists. This heterologous desensitization occurred within 15 min and persisted for days, with gradual recovery of cAMP responses roughly paralleling those of cells from patients with atopic dermatitis. These findings provide a possible explanation for Szentivanyi's beta adrenergic blockade theory and the depressed leukocyte cAMP response to multiple agonists in atopy.
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U2 - 10.1016/0091-6749(81)90187-1
DO - 10.1016/0091-6749(81)90187-1
M3 - Article
C2 - 6114971
AN - SCOPUS:0019478760
SN - 0091-6749
VL - 68
SP - 218
EP - 225
JO - The Journal of Allergy and Clinical Immunology
JF - The Journal of Allergy and Clinical Immunology
IS - 3
ER -