Role of interleukin-13 in eosinophil accumulation and airway remodelling in a mouse model of chronic asthma

Clin Exp Allergy. 2002 Jul;32(7):1104-11. doi: 10.1046/j.1365-2222.2002.01420.x.


Background: Interleukin-13 is believed to be important in asthmatic inflammation and airway hyper-reactivity.

Objective: To investigate the role of IL-13 in chronic asthma, using an improved experimental model of asthma that reproduces most of the morphological features of the human disease.

Methods: BALB/c mice or gene-targeted mice deficient in their ability to produce IL-13 or the IL-4 receptor alpha-chain (IL-4Ralpha) were sensitized to ovalbumin and exposed to aerosolized antigen for 30 min/day on 3 days/week for 6 weeks. Intraepithelial eosinophils, accumulation of chronic inflammatory cells in the airway wall, subepithelial fibrosis, epithelial hypertrophy and numbers of mucous cells were quantified histomorphometrically. Airway hyper-reactivity (AHR) to a cholinergic agonist was assessed by barometric plethysmography.

Results: Compared with wild-type animals, IL-13 -/- mice exhibited diminished accumulation of eosinophils and chronic inflammatory cells, as well as reduced subepithelial fibrosis, epithelial hypertrophy and mucous cell hyperplasia (P < 0.01 for all comparisons). In contrast, AHR was still demonstrable in IL -13 -/- mice. In IL-4Ralpha -/- mice the inflammatory response, subepithelial fibrosis and AHR were similar to wild-type mice, although the receptor-deficient mice had significantly less epithelial hypertrophy and mucous cell hyperplasia.

Conclusion: These results imply a critical role for IL-13 in accumulation of intraepithelial eosinophils in chronic asthma, as well as in epithelial and subepithelial remodelling. In addition, they suggest that in chronic asthma, IL-13 may be capable of signalling via a pathway that does not involve IL-4Ralpha.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Asthma / pathology*
  • Bronchial Hyperreactivity / etiology
  • Chronic Disease
  • Disease Models, Animal
  • Eosinophils / physiology*
  • Epithelium / pathology
  • Female
  • Fibrosis
  • Interleukin-13 / physiology*
  • Mice
  • Mice, Inbred BALB C
  • Receptors, Interleukin-4 / physiology
  • Trachea / pathology*


  • Interleukin-13
  • Receptors, Interleukin-4