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

By S. Molet, Q. Hamid, Francis Davoineb, E. Nutku, Rame Tahaa, N. Pagé, R. Olivenstein, J. Elias, J. Chakir. Journal of Allergy and Clinical Immunology, 2001

1,037 citations recorded by the source corpus.

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.

Subfields: Dermatology, Immunology, Physiology

View Paper: https://www.semanticscholar.org/paper/4246b1294e5276d5d30ca30544a935667660c602

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Citations in the corpus

Interleukin-17 family and IL-17 receptors. (2003, background): “↑ IL-11 mRNA only in asthmatic patients Dexamethasone inhibits IL-17A-induced IL-6, IL-11 No effect of IL-17A on IL-11 in non-asthma [91]”
IL-17 mRNA in sputum of asthmatic patients: linking T cell driven inflammation and granulocytic influx? (2006, background): “IL-17 is especially important for the recruitment of neutrophils [12] and is expressed in bronchial biopsies, bronchoalveolar lavage fluid and sputum of patients with asthma [13-15].”
IL-17 and Th17 Cells. (2009, background): “Nevertheless, good circumstantial evidence suggests that Th17 cells are important in human psoriasis (114), rheumatoid arthritis (115), multiple sclerosis (116), inflammatory bowel disease (92), asthma (117, 118), and some bacterial and fungal infections.”
IL-17-Mediated Regulation of Innate and Acquired Immune Response against Pulmonary Mycobacterium bovis Bacille Calmette-Guérin Infection1 (2007, background): “thritis (21, 22), allograft rejection (23, 24), and asthma (25, 26).”