Scientists have opened up a possible new approach to understanding bronchospasm in asthma sufferers with the finding that many patients with airway obstruction have substantial amounts of antibody to the receptor that, when bound to epinephrine, produces bronchial relaxation.
The search for such autoantibodies became possible when the cell receptor involved, the β2-adrenergic receptor, was purified in the laboratory of J. Craig Venter, PhD, of the Department of Pharmacology and Therapeutics at the State University of New York at Buffalo.
In healthy persons, epinephrine binding to the β2-adrenergic receptor causes bronchial smooth muscle to relax. However, in persons with asthma, according to one prevailing theory, bronchospasm may occur because these receptors are less sensitive to epinephrine.
Venter and colleagues reasoned that this loss of sensitivity might be caused in some persons by antibodies to the receptor, just as myasthenia gravis is most likely caused by antibodies