No conflicts of interest were declared.
IL-32 up-regulation is associated with inflammatory cytokine production in allergic rhinitis†
Article first published online: 19 MAY 2011
Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Journal of Pathology
Volume 224, Issue 4, pages 553–563, August 2011
How to Cite
Jeong, H.-J., Shin, S.-Y., Oh, H.-A., Kim, M.-H., Cho, J.-S. and Kim, H.-M. (2011), IL-32 up-regulation is associated with inflammatory cytokine production in allergic rhinitis. J. Pathol., 224: 553–563. doi: 10.1002/path.2899
- Issue published online: 4 JUL 2011
- Article first published online: 19 MAY 2011
- Accepted manuscript online: 15 MAR 2011 12:00AM EST
- Manuscript Accepted: 11 MAR 2011
- Manuscript Revised: 10 FEB 2011
- Manuscript Received: 8 NOV 2010
- allergic rhinitis;
- granulocyte-macrophage colony-stimulating factor;
- inflammatory cytokines
IL-32 is a described pro-inflammatory cytokine produced by T lymphocytes, natural killer cells, monocytes, and epithelial cells. However, the specific mechanism of IL-32 on allergic rhinitis (AR) has not been elucidated. Here, we report a significant increase of IL-32 protein and mRNA in the nasal mucosa of AR patients. In addition, in nasal mucosa tissue from AR patients, the level of IL-32 production correlated with inflammation, IL-1β, IL-18, and granulocyte-macrophage colony-stimulating factor (GM-CSF). In an AR animal model, IL-32 significantly increased IgE and inflammatory cytokine levels. IL-32 expression was induced by recombinant human GM-CSF via activation of caspase-1 in eosinophils. In addition, depletion of IL-32 prevents the production of inflammatory cytokines in eosinophils. In conclusion, IL-32 is an important cytokine involved in the inflammation of AR. The regulation of IL-32 expression may form the basis of a new strategy for the treatment of AR. Copyright © 2011 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.