Receptors in airway disease. Beta-adrenoceptors in lung inflammation

Beta-adrenoceptor dysfunction and increase in airway reactivity can be induced by administration of gram-negative bacteria, endotoxin, viruses, and allergens in laboratory animals. However, the deterioration of lung beta-adrenoceptor function is not invariably associated with lung inflammation. Severe asthmatics, but not asthmatics per se, show a diminished beta-adrenoceptor function of airway smooth muscle. These changes are probably a consequence of the active disease state rather than an intrinsic component of asthma. Mediators released from inflammatory cells such as reactive oxygen species and fatty acid metabolites may directly or indirectly induce beta-adrenoceptor dysfunction. Beta-adrenoceptor function of leukocytes from asthmatic patients can be decreased as well and it is suggested that lymphokines like interleukin-2 and interferon-gamma may affect beta-adrenoceptor function. A disturbed beta-adrenoceptor function on inflammatory cells themselves may have consequences for their immune function, mediator release, and effect on surrounding tissues.