TY - JOUR
T1 - The effect of IL-13 and IL-13R130Q, a naturally occuring IL-13 polymorphism, on the gene expression of human airway smooth muscle cells
AU - Syed, Farhat
AU - Panettieri, Reynold A.
AU - Tliba, Omar
AU - Huang, Chris
AU - Li, Katherine
AU - Bracht, Michelle
AU - Amegadzie, Bernard
AU - Griswold, Don
AU - Li, Li
AU - Amrani, Yassine
PY - 2005/1/20
Y1 - 2005/1/20
N2 - Background: Growing evidence shows that interleukin 13 (IL-13) may play an essential role in the development of airway inflammation and bronchial hyper-responsiveness (BHR), two defining features of asthma. Although the underlying mechanisms remain unknown, a number of reports have shown that IL-13 may exert its deleterious effects in asthma by directly acting on airway resident cells, including epithelial cells and airway smooth muscle cells. In this report, we hypothesize that IL-13 may participate in the pathogenesis of asthma by activating a set of "proasthmatic" genes in airway smooth muscle (ASM) cells. Methods: Microarray technology was used to study the modulation of gene expression of airway smooth muscle by IL-13 and IL-13R130Q. TaqMan™ Real Time PCR and flow cytometry was used to validate the gene array data. Results: IL-13 and the IL-13 polymorphism IL-13R130Q (Arg130Gln), recently associated with allergic asthma, seem to modulate the same set of genes, which encode many potentially interesting proteins including vascular cellular adhesion molecule (VCAM)-1, IL-13Rα2, Tenascin C and Histamine Receptor H1, that may be relevant for the pathogenesis of asthma. Conclusions: The data supports the hypothesis that gene modulation by IL-13 in ASM may be essential for the events leading to the development of allergic asthma.
AB - Background: Growing evidence shows that interleukin 13 (IL-13) may play an essential role in the development of airway inflammation and bronchial hyper-responsiveness (BHR), two defining features of asthma. Although the underlying mechanisms remain unknown, a number of reports have shown that IL-13 may exert its deleterious effects in asthma by directly acting on airway resident cells, including epithelial cells and airway smooth muscle cells. In this report, we hypothesize that IL-13 may participate in the pathogenesis of asthma by activating a set of "proasthmatic" genes in airway smooth muscle (ASM) cells. Methods: Microarray technology was used to study the modulation of gene expression of airway smooth muscle by IL-13 and IL-13R130Q. TaqMan™ Real Time PCR and flow cytometry was used to validate the gene array data. Results: IL-13 and the IL-13 polymorphism IL-13R130Q (Arg130Gln), recently associated with allergic asthma, seem to modulate the same set of genes, which encode many potentially interesting proteins including vascular cellular adhesion molecule (VCAM)-1, IL-13Rα2, Tenascin C and Histamine Receptor H1, that may be relevant for the pathogenesis of asthma. Conclusions: The data supports the hypothesis that gene modulation by IL-13 in ASM may be essential for the events leading to the development of allergic asthma.
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U2 - 10.1186/1465-9921-6-9
DO - 10.1186/1465-9921-6-9
M3 - Article
C2 - 15661077
AN - SCOPUS:25444487989
SN - 1465-993X
VL - 6
JO - Respiratory Research
JF - Respiratory Research
M1 - 9
ER -