Am. J. Respir. Crit. Care Med., Vol 154, No. 5, 11 1996, 1272-1276.
Incubation with IgE increases cholinergic neurotransmission in human airways in vitro
M Ichinose, M Miura, M Tomaki, T Oyake, N Kageyama, Y Ikarashi, Y Maruyama and K Shirato
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Airway cholinergic hyperresponsiveness is frequently observed in asthmatic
patients. Recent reports suggest the possible involvement of IgE in
hyperresponsiveness, although the exact mechanism is still uncertain. In
this study, we examined whether incubation with IgE could facilitate the
cholinergic function in human airways. Bronchi were obtained from 20
patients undergoing lung resection. Cholinergic contractile responses were
induced by electrical field stimulation (EFS) or exogenous acetylcholine
(ACh), and they were assessed by isometric tension measurement. EFS-induced
ACh release from cholinergic nerves was also measured by high performance
liquid chromatography. Incubation with IgE significantly enhanced
EFS-induced bronchial contraction and ACh release as compared with the
values of the bronchi incubated with heat inactivated IgE (control) (p <
0.05, respectively), but it did not alter the contractile responses induced
by exogenous ACh. Pretreatment with the muscarinic M2-receptor agonist
pilocarpine reduced the EFS-induced ACh release in the control tissues (p
< 0.05), but not in the tissues incubated with IgE. The M2-receptor
antagonist methoctramine significantly enhanced the EFS-induced contraction
in control bronchi (p < 0.05), but this augmentation was not observed in
the tissues incubated with IgE. These results suggest that IgE itself can
enhance cholinergic bronchial contraction via facilitation of ACh release
from cholinergic nerves and that this augmentation is related to
autoreceptor M2 dysfunction at nerve endings.
