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Division of Respiratory Medicine, City Hospital, University of Nottingham, Nottingham NG5 1PB, United Kingdom
Interleukin
(IL)-1
impairs human airway smooth muscle (ASM) cell cAMP responses
to isoproterenol (Iso). We investigated if bradykinin (BK) could cause
a similar effect and the role of cyclooxygenase (COX) products in this
event, since we have recently reported that BK, like IL-1, also
causes COX-2 induction and prostanoid release in human ASM cells. BK
pretreatment significantly attenuated Iso-induced cAMP generation in a
time- and concentration-dependent manner. cAMP generation by
prostaglandin (PG) E2 but not by
forskolin was also impaired. The COX inhibitor indomethacin completely
prevented the impairment, whereas the selective COX-2 inhibitors NS-398 and nimesulide, protein synthesis inhibitors cycloheximide and actinomycin D, and steroid dexamethasone were all partially effective. The impairment was mimicked by the
B2 agonist
[Tyr(Me)8]BK, the
Ca2+ ionophore A-23187, and
PGE2 and prevented by the
B2 antagonist HOE-140, but
anti-IL-1 serum was ineffective. The results indicate that BK
impairs human ASM cell responses to Iso, and the effect is largely
mediated by B2 receptor-related
COX product release via both COX isoforms and is independent of
IL-1.
airway inflammation; prostaglandin E2; asthma; cyclooxygenase induction; isoproterenol; adenosine 3',5'-cyclic monophosphate
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