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- Title
Human eosinophils release IL-1ß and increase expression of IL-17A in activated CD4<sup>+</sup> T lymphocytes.
- Authors
Esnault, S.; Kelly, E. A. B.; Nettenstrom, L. M.; Cook, E. B.; Seroogy, C. M.; Jarjour, N. N.
- Abstract
Background Differentiation and activation of CD4+ T cells is controlled by various cytokines produced by innate immune cells. We have shown that eosinophils ( EOS) have the potential to influence Th1 and Th2 cytokine generation by CD4+ cells, but their influence on IL-17A ( IL-17) has not been established. Objective The purpose of this study is to determine the effect of EOS on IL-17 production by lymphocytes. Methods Pre-activated CD4+ T cells were cultured in the presence of either autologous EOS or EOS culture supernatants. Expression of IL-17 was determined by real-time quantitative PCR ( qPCR) after 5 h and protein level was measured after 48 h. To determine the effect of allergen-induced airway EOS on IL-17, subjects with mild allergic asthma underwent bronchoscopic segmental bronchoprovocation with allergen (SBP-Ag) after a treatment with an anti-IL-5 neutralizing antibody (mepolizumab) to reduce airway eosinophilia. IL-17 mRNA was measured in bronchoalveolar lavage (BAL) cells by qPCR. Results In vitro, EOS significantly increased IL-17 production by CD4+ T cells. Addition of exogenous IL-1ß increased expression of IL-17 mRNA by CD4+ T cells. EOS expressed and released IL-1ß. Furthermore, levels of IL-1ß in EOS supernatants highly correlated with their ability to increase IL-17 expression by CD4+ T cells, and neutralizing antibody to IL-1ß reduced expression of IL-17 mRNA. In vivo, reduction of EOS in the airway using mepolizumab was associated with diminished IL-17 expression after SBP-Ag. Conclusions and clinical relevance Our data demonstrate that EOS can promote IL-17 production through the release of IL-1ß. Enhanced IL-17 cytokine production is another mechanism by which EOS may participate in pathogenesis of allergic airway inflammation in asthma.
- Publication
Clinical & Experimental Allergy, 2012, Vol 42, Issue 12, p1756
- ISSN
0954-7894
- Publication type
Academic Journal
- DOI
10.1111/j.1365-2222.2012.04060.x