Edited by: Hans-Uwe Simon
Differential expression of interleukin-32 in chronic rhinosinusitis with and without nasal polyps
Article first published online: 7 SEP 2011
© 2011 John Wiley & Sons A/S
Volume 67, Issue 1, pages 25–32, January 2012
How to Cite
Keswani, A., Chustz, R. T., Suh, L., Carter, R., Peters, A. T., Tan, B. K., Chandra, R., Kim, S.-H., Azam, T., Dinarello, C. A., Kern, R. C., Schleimer, R. P. and Kato, A. (2012), Differential expression of interleukin-32 in chronic rhinosinusitis with and without nasal polyps. Allergy, 67: 25–32. doi: 10.1111/j.1398-9995.2011.02706.x
- Issue published online: 12 DEC 2011
- Article first published online: 7 SEP 2011
- Accepted for publication 9 August 2011
- chronic rhinosinusitis;
- epithelial cells;
- T lymphocytes
To cite this article: Keswani A, Chustz RT, Suh L, Carter R, Peters AT, Tan BK, Chandra R, Kim S-H, Azam T, Dinarello CA, Kern RC, Schleimer RP, Kato A. Differential expression of interleukin-32 in chronic rhinosinusitis with and without nasal polyps. Allergy 2012; 67: 25–32.
Background: Chronic rhinosinusitis (CRS) is a heterogeneous disease characterized by local inflammation of the upper airways and sinuses and is frequently divided into polypoid CRS (CRSwNP) and nonpolypoid CRS (CRSsNP). However, the mechanism of inflammation in CRS has still not been fully elucidated. The aim of the study was to investigate the role of interleukin-32 (IL-32), a recently discovered proinflammatory cytokine, in CRS.
Methods: We collected nasal epithelial cells and nasal tissue from patients with CRS and control subjects. We assayed mRNA for IL-32 by real-time PCR and measured IL-32 protein using ELISA, Western blot, and immunohistochemistry.
Results: The expression of mRNA for IL-32 was elevated in epithelial cells from uncinate tissue from patients with CRSsNP compared with patients with CRSwNP (P < 0.05), control subjects (P = 0.06), and epithelial cells from nasal polyp (NP) tissue (P < 0.05). Production of IL-32 was induced by IFN-γ, TNF, and dsRNA in primary airway epithelial cells. In whole-tissue extracts, the expression of IL-32 protein was significantly elevated in patients with CRSwNP compared with patients with CRSsNP and control subjects. Immunohistochemistry data showed that IL-32 was detected in mucosal epithelial cells and inflammatory cells in the lamina propria. Levels of IL-32 were correlated with the levels of CD3 and macrophage mannose receptor in NP tissue. Immunofluorescence data showed IL-32 co-localization with CD3-positive T cells and CD68-positive macrophages in NPs.
Conclusion: Overproduction of IL-32 may be involved in the pathogenesis of CRS, although the role of IL-32 in the inflammation in CRSsNP and CRSwNP may be different.