| pubmed-article:6254414 | pubmed:abstractText | Rhinovirus respiratory infections have been frequently associated with the precipitation of an asthma attack. As an explanation for virus-provoked asthma, it has been proposed that viruses or their products may alter beta-adrenergic responsiveness. Isolated human granulocytes have provided an in vitro study model for this problem. Granulocyte release of the lysosomal enzyme beta-glucuronidase (BG) occurred after incubation with complement-activated zymosan particles, and this release was inhibited by isoproterenol (ISO), histamine (HIS) acting via its H2 receptor, and prostaglandin E1 (PGE1). In asthma, the granulocyte response to HIS and ISO was impaired, and the ISO impairment was accentuated during virus-provoked asthma. After an in vitro incubation of polymorphonuclear leukocytes (PMN) with rhinovirus 16, the granulocyte response to ISO, HIS, and PGE1 was significantly reduced. This change in agonist response was proportional to the virus dosage, maximal at 37 degrees C and after a 60-min incubation period, and occurred with heat or UV-inactivated virus. It is possible that impaired beta-adrenergic responsiveness may also develop in other tissues, such as the airway smooth muscle, and thus explain, in part, wheezing during viral respiratory infections. | lld:pubmed |
