Increased tachykinin receptor gene expression in asthmatic lung and its modulation by steroids.
Substance P has several inflammatory effects on the airways mediated via neurokinin 1 receptors (NK1Rs) and, if released from sensory nerves, may amplify the chronic inflammation seen in asthma. Northern blot analysis of NK1R mRNA in lung showed a 52 +/- 10% (S.E.M.; P < 0.01) increase in mRNA in the asthmatic lung compared with non-asthmatic control tissue. NK1R mRNA was reduced by 84.5 +/- 1.9% after incubation with dexamethasone (1 microM) for 3 h (P < 0.01). In contrast, NK2R mRNA was unaltered in asthmatic lungs and dexamethasone treatment had no effect on the level of NK2R mRNA. These results suggest that chronic inflammation in asthma may result in increased NK1R gene expression and that this effect is reversed by glucocorticosteroids.
Adcock
I M
IM
Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.
Peters
M
M
Gelder
C
C
Shirasaki
H
H
Brown
C R
CR
Barnes
P J
PJ
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000378:metabolism*; D015152:Blotting, Northern; D002648:Child; D003907:Dexamethasone / Q000494:pharmacology; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008168:Lung / Q000187:drug effects / Q000378:metabolism*; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D018040:Receptors, Neurokinin-1 / Q000096:biosynthesis*; D012016:Reference Values
D012333:RNA, Messenger; D018040:Receptors, Neurokinin-1; D003907:Dexamethasone