The cholinergic system in rat and human airways and the effects of
glucocorticoids were investigated by assay of
choline acetyltransferase activity, by high-pressure liquid chromatography measurement of
acetylcholine, and by anti-
choline acetyltransferase immunocyto-/histochemistry. Human bronchi were obtained at surgery from patients with
lung cancer. Group 1 patients did not suffer from additional
lung diseases and had not been treated with
glucocorticoids. Group 2 patients, who suffered in addition to
lung cancer from chronic obstructive
bronchitis, had been treated for at least 6 weeks before surgery with four puffs of
flusinolid daily. Isolated bronchial epithelial cells as well as intact surface epithelium of human bronchi expressed
choline acetyltransferase immunoreactivity and
choline acetyltransferase enzyme activity (3 +/- 1 nmol/mg protein per h). Ciliated epithelial cells showed strong
choline acetyltransferase immunoreactivity at the basal body and the roolet of cilia. Surface epithelium in group 1 and 2 bronchi contained 23 +/- 6 (n = 14) and 1.8 +/- 0.3 pmol/g
acetylcholine) (n = 7, P < 0.001), respectively, whereas the transmural
acetylcholine content did not differ significantly between both groups. The amount of
choline acetyltransferase immunoreactivity appeared similar in the surface epithelium of both groups. In an animal (rat) study the effects of oral
dexamethasone (3 mg/day, 1 week) on
choline acetyltransferase activity and
acetylcholine levels were investigated.
Dexamethasone treatment reduced epithelial
acetylcholine in the airways and small intestine by about 80% and inhibited epithelial
choline acetyltransferase activity. In conclusion, epithelial cells of human airways possess components of the cholinergic system, i.e., contain the synthesizing enzyme
choline acetyltransferase and store
acetylcholine. The data obtained from the animal study indicate that
glucocorticoids can inhibit epithelial
acetylcholine.