The effect of IL-13 and IL-13R130Q, a naturally occurring IL-13 polymorphism, on the gene expression of human airway smooth muscle cells

Respir Res. 2005 Jan 20;6(1):9. doi: 10.1186/1465-9921-6-9.

Abstract

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 "pro-asthmatic" 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-13Ralpha2, 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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cells, Cultured
  • DNA Mutational Analysis
  • Gene Expression Profiling
  • Genetic Predisposition to Disease / genetics
  • Humans
  • Interleukin-13 / genetics*
  • Interleukin-13 / metabolism*
  • Myocytes, Smooth Muscle / metabolism*
  • Polymorphism, Genetic
  • Trachea / metabolism*
  • Vascular Cell Adhesion Molecule-1 / metabolism*

Substances

  • Interleukin-13
  • Vascular Cell Adhesion Molecule-1