IL-13 mRNA and immunoreactivity in allergen-induced rhinitis: comparison with IL-4 expression and modulation by topical glucocorticoid therapy

Am J Respir Cell Mol Biol. 1997 Jul;17(1):17-24. doi: 10.1165/ajrcmb.17.1.2696.


The allergen-induced late nasal response (LNR) is associated with high expression of interleukin-4 (IL-4) and IL-5 messenger RNA (mRNA) in the nasal mucosa, suggesting a role for Th2-type cytokines in the development of the LNR. Moreover, topical corticosteroid-mediated inhibition of the LNR is accompanied by inhibition of IL-4, but not IL-5, mRNA expression, IL-13 shares a number of functions with IL-4, including IgE switching and vascular cell adhesion molecule-1 (VCAM-1) upregulation. We investigated the expression of IL-13 mRNA and immunoreactivity in nasal biopsies from 10 normal subjects and 20 subjects with allergic rhinitis. IL-4 mRNA expression was examined in the same subjects. The allergic rhinitis patients were randomized to receive a 6-wk treatment with either topical fluticasone propionate (n = 10) or placebo (n = 10) nasal spray twice daily. A nasal biopsy was taken before treatment and 24 h after local nasal allergen provocation with a grass-pollen extract. Before treatment, there was no significant difference between the allergic rhinitis patients and controls in the expression of IL-13 mRNA and immunoreactivity. After allergen provocation, we observed a significant increase in IL-13 mRNA-positive and immunoreactive cells at 24 h only in subjects given placebo (P < 0.001). Inhibition of the LNR after corticosteroid treatment was associated with a marked decrease in allergen-induced IL-13 mRNA-positive (P < 0.001) and immunoreactive cells (P < 0.001). In subjects given placebo, 76.9 +/- 5.5% of IL-13 mRNA-positive cells observed after allergen were CD3+, whereas 11.2 +/- 2.7% coexpressed immunoreactivity for mast-cell tryptase. In these subjects, increases in cells expressing IL-13 mRNA were greater than for IL-4 mRNA (P = 0.001), and double in situ hybridization studies revealed that 100% of the IL-4 mRNA-positive cells coexpressed IL-13 mRNA, whereas 66.6 +/- 10.5% of IL-13 mRNA-positive cells coexpressed IL-4 transcripts after allergen challenge. The results of this study suggest that IL-13 expression is a prominent feature of the LNR, and that inhibition of the LNR following steroid therapy may be partly attributable to inhibition of IL-13 expression.

Publication types

  • Clinical Trial
  • Comparative Study
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Intranasal
  • Adult
  • Allergens
  • Androstadienes / administration & dosage
  • Androstadienes / therapeutic use*
  • Anti-Allergic Agents / administration & dosage
  • Anti-Allergic Agents / therapeutic use
  • Anti-Inflammatory Agents / administration & dosage
  • Anti-Inflammatory Agents / therapeutic use*
  • Biopsy
  • CD3 Complex / analysis
  • Chymases
  • Female
  • Fluticasone
  • Glucocorticoids
  • Humans
  • Interleukin-13 / biosynthesis*
  • Interleukin-4 / biosynthesis*
  • Male
  • Mast Cells / enzymology
  • Nasal Mucosa / drug effects
  • Nasal Mucosa / immunology*
  • Nasal Mucosa / pathology
  • Placebos
  • RNA, Messenger / biosynthesis*
  • Reference Values
  • Rhinitis, Allergic, Seasonal / drug therapy*
  • Rhinitis, Allergic, Seasonal / immunology*
  • Serine Endopeptidases / biosynthesis
  • Transcription, Genetic* / drug effects
  • Tryptases


  • Allergens
  • Androstadienes
  • Anti-Allergic Agents
  • Anti-Inflammatory Agents
  • CD3 Complex
  • Glucocorticoids
  • Interleukin-13
  • Placebos
  • RNA, Messenger
  • Interleukin-4
  • Fluticasone
  • Serine Endopeptidases
  • chymase 2
  • Chymases
  • Tryptases