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- W1798981858 abstract "IL-13 modulates airway smooth muscle sensitivity to contractile stimulus. Steroids and β2 adrenoceptor (AR) agonists decrease inflammation and inhibit airway hyper-responsiveness (AHR) in asthma. We postulate that steroids decrease AHR after IL-13 stimulation, and IL-13 alters bronchodilation of small airways. Precision cut lung slices (PCLS) from disease-free donors were incubated with 100 ng/mL IL-13 (18 h) and examined for carbachol (Cch)-induced bronchoconstriction, and formoterol- (Form) or forskolin (Fsk)-induced bronchodilation. To assess the effect of steroids, slices were preincubated with budesonide (Bud) for 1 h prior to IL-13. Data shown are mean % change of baseline luminal area ± sem. IL-13 significantly increased bronchoconstriction to a maximal effective concentration (100 μM) of Cch (Control (C): -80 ± 4, IL-13: -89 ± 3, p=0.02) and decreased the bronchodilation to 0.3 nM Form (C: 54 ± 8, IL-13: 20 ± 4, p These data suggest that pretreatment with budesonide completely prevents the effects of IL-13 on both airway contractility and adenylyl cyclase-mediated bronchodilation but does not prevent the IL-13-induced impairment of β2AR agonist-mediated bronchodilation. Further studies will define the underlying mechanisms by which IL-13 attenuates β2AR-mediated bronchodilation." @default.
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- W1798981858 date "2012-09-01" @default.
- W1798981858 modified "2023-09-26" @default.
- W1798981858 title "Budesonide reverses IL-13-induced airway hyper-responsiveness but has little effect on β2 agonist response in human small airways" @default.
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