IL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines

J Allergy Clin Immunol. 2001 Sep;108(3):430-8. doi: 10.1067/mai.2001.117929.


Background: IL-17 is a cytokine that has been reported to be produced by T lymphocytes. In vitro, IL-17 activates fibro-blasts and macrophages for the secretion of GM-CSF, TNF-alpha, IL-1beta, and IL-6. A number of these cytokines are involved in the airway remodeling that is observed within the lungs of asthmatic individuals.

Objective: In this study, we investigated the expression of IL-17 in sputum and bronchoalveolar lavage specimens obtained from asthmatic subjects and from nonasthmatic control subjects.

Methods: IL-17 was detected through use of immunocytochemistry, in situ hybridization, and Western blot. Bronchial fibroblasts were stimulated with IL-17, and cytokine production and chemokine production were detected through use of ELISA and RT-PCR.

Results: Using immunocytochemistry, we demonstrated that the numbers of cells positive for IL-17 are significantly increased in sputum and bronchoalveolar lavage fluids of subjects with asthma in comparison with control subjects (P <.001 and P <.005, respectively). We demonstrated that in addition to T cells, eosinophils in sputum and bronchoalveolar lavage fluids expressed IL-17. Peripheral blood eosinophils were also positive for IL-17, and the level of IL-17 in eosinophils purified from peripheral blood was significantly higher in subjects with asthma than in controls (P <.01). To further investigate the mechanism of action of IL-17 in vivo, we examined the effect of this cytokine on fibroblasts isolated from bronchial biopsies of asthmatic and nonasthmatic subjects. IL-17 did enhance the production of pro-fibrotic cytokines (IL-6 and IL-11) by fibroblasts, and this was inhibited by dexamethasone. Similarly, IL-17 increased the level of other fibroblast-derived inflammatory mediators, such as the alpha-chemokines, IL-8, and growth-related oncogene-alpha.

Conclusion: Our results, which demonstrate for the first time that eosinophils are a potential source of IL-17 within asthmatic airways, suggest that IL-17 might have the potential to amplify inflammatory responses through the release of proinflammatory mediators such as alpha-chemokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Asthma / immunology*
  • Bronchi / cytology
  • Bronchi / drug effects*
  • Bronchoalveolar Lavage Fluid / immunology
  • Chemokine CXCL1
  • Chemokines, CXC*
  • Chemotactic Factors / biosynthesis
  • Cytokines / metabolism*
  • Eosinophils / immunology
  • Female
  • Fibroblasts / cytology
  • Fibroblasts / drug effects*
  • Growth Substances / biosynthesis
  • Humans
  • Intercellular Signaling Peptides and Proteins*
  • Interleukin-11 / metabolism
  • Interleukin-17 / isolation & purification
  • Interleukin-17 / pharmacology*
  • Interleukin-6 / metabolism
  • Interleukin-8 / biosynthesis
  • Male
  • Sputum / immunology


  • CXCL1 protein, human
  • Chemokine CXCL1
  • Chemokines, CXC
  • Chemotactic Factors
  • Cytokines
  • Growth Substances
  • Intercellular Signaling Peptides and Proteins
  • Interleukin-11
  • Interleukin-17
  • Interleukin-6
  • Interleukin-8