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Regulation and expression of IL-32 in chronic rhinosinusitis
M B Soyka1, A Treis, T Eiwegger
1Swiss Institute of Allergy and Asthma Research, University of Zurich, Davos, Switzerland.
Allergy
|April 11, 2012
Summary
Interleukin-32 (IL-32) is upregulated by specific cytokines and T cells in chronic rhinosinusitis (CRS). Increased IL-32 expression in nasal tissues suggests its role in CRS pathogenesis.
Area of Science:
- Immunology
- Inflammation Research
- Otolaryngology
Background:
- Activated T lymphocytes and epithelial cell interactions are key in chronic rhinosinusitis (CRS) inflammation.
- Interleukin-32 (IL-32) is a cytokine implicated in various chronic inflammatory diseases.
Purpose of the Study:
- To investigate the role and expression of IL-32 in the pathogenesis of CRS.
- To determine the regulation of IL-32 by cytokines and T cells in sinonasal epithelial cells.
Main Methods:
- Primary human sinonasal epithelial cells (HSECs) were stimulated with cytokines.
- IL-32 mRNA and protein expression were analyzed via real-time PCR, Western blot, and flow cytometry.
- Nasal biopsies from CRS patients and healthy controls were examined for IL-32 expression.
Main Results:
- Tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) upregulated IL-32 mRNA in HSECs.
- IL-32 mRNA expression was higher in HSECs co-cultured with Th1 cells compared to Th0 or Th2 cells.
- Significantly higher IL-32 mRNA and protein levels were found in sinonasal tissues of CRS patients with nasal polyps compared to controls.
Conclusions:
- IL-32 is induced by TNF-α, IFN-γ, and Th1 cells.
- Elevated IL-32 expression in CRS tissues indicates its potential involvement in CRS pathogenesis.
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