IL‐13 enhances agonist‐evoked calcium signals and contractile responses in airway smooth muscle

Growing evidence suggests that interleukin (IL)‐13, a Th2‐type cytokine, plays a critical role in the development of bronchial hyper‐responsiveness (BHR), an essential feature of asthma, although the underlying mechanisms remain unknown. In the present study, we investigated whether IL‐13 directly a...

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Bibliographic Details
Published in:British journal of pharmacology 2003-12, Vol.140 (7), p.1159-1162
Main Authors: Tliba, Omar, Deshpande, Deepak, Chen, Hang, Van Besien, Christopher, Kannan, Mathur, Panettieri, Reynold A, Amrani, Yassine
Format: Article
Language:English
Subjects:
airway smooth muscle
Animals
Asthma
Biological and medical sciences
Bradykinin - pharmacology
Calcium - metabolism
Calcium Signaling - drug effects
Carbachol - pharmacology
Cells, Cultured
Cytosol
Dose-Response Relationship, Drug
Histamine - pharmacology
Humans
Interleukin-13 - pharmacology
isometric tension
Medical sciences
Mice
Muscle Contraction - drug effects
Muscle, Smooth - drug effects
Pharmacology. Drug treatments
Potassium Chloride - pharmacology
Recombinant Proteins - pharmacology
Special Reports
Th2 cytokine
Trachea - drug effects
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Summary:Growing evidence suggests that interleukin (IL)‐13, a Th2‐type cytokine, plays a critical role in the development of bronchial hyper‐responsiveness (BHR), an essential feature of asthma, although the underlying mechanisms remain unknown. In the present study, we investigated whether IL‐13 directly affects airway smooth muscle (ASM) function. In murine tracheal rings, IL‐13 (100 ng ml−1, 24 h) significantly increased both the carbachol‐ and KCl‐induced maximal force generation without affecting ASM sensitivity. In cultured human ASM cells, IL‐13 (50 ng ml−1, 24 h) also augmented cytosolic calcium levels to bradykinin, histamine and carbachol by 60, 35 and 26%, respectively. The present study demonstrates that IL‐13 may promote BHR by directly modulating ASM contractility, an effect that may be due to enhanced G protein‐coupled receptor (GPCR)‐associated calcium signaling. British Journal of Pharmacology (2003) 140, 1159–1162. doi:10.1038/sj.bjp.0705558
ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0705558