Some alterations of the leucoeyte β2-adrenoceptor/cAMP-system in patients with seasonal allergic rhinoconjunctivitis are related to disease activity


Priv.-Doz. Dr. E. Haen, Walther-Straub-lnstitut für Pharmakologie und Toxikoiogie. Nussbaumstr. 26, D-80336 M%uUnchen, Germany.


Background Disturbances of β2-adrenoceptors are discussed as a pathogenic factor in atopic diseases.

Methods In this study tbe expression and function of β2-adrenoceptors on peripheral blood leucocytes (PBL) of seven atopic patients with seasonal rhinoconjunctivitis and their seven healthy controls was evaluated in relation to disease activity. Earlier reported data during pollen. season were now compared with data obtained from the same subjects after their allergic symptoms had subsided.

Results The variables that had indicated a β2-adrenoceptor subsensitivity in tbe patients during pollen season returned to control values, i.e. the reduced β2-adrenoceptor affinity, the reduced β2-adrenoceptor sensitivity, the reduced increase of intracellular cyclic adenosine monophosphate (cAMP) content upon stimulation with isoproterenol, and the reduced cAMP plasma concentration (values no longer significantly different from those of controls). However, the variable that had suggested an increase in activity of the cAMP degrading enzyme phosphodiesterase (PDE), i.e. the reduced basal intracellular cAMP content of the patients, remained reduced after the pollen season (4.9 ± 1.1 pmol/lO6’cells in patients vs 8.2 ± 0.9pmol/106 cells in controls: P < 0.05). There were no significant differences in β2-adrenoceptor density between patients and controls at both investigations.

Conclusions Atopic seasonal rhinoconjunctivitis is associated with various alterations in the PBL β2-adrenoceptor/cAMP system that depend on disease activity. The reversible β2-adrenoceptor subsensitivity is likely to be a consequence of the disease, whereas the irreversibly decreased basal intracellular cAMP content, suggested an elevated PDE activity, might be a basic trait of atopy.