Guimin Zhang and Xiang Jing contributed equally to this work.
Contribution of the Proinflammatory Cytokine IL-18 in the Formation of Human Nasal Polyps†
Article first published online: 28 APR 2011
Copyright © 2011 Wiley-Liss, Inc.
The Anatomical Record
Volume 294, Issue 6, pages 953–960, June 2011
How to Cite
Zhang, G., JING, X., Wang, X., Shi, W., Sun, P., Su, C., Zhu, M., Yang, Z., Yao, Z. and Yang, J. (2011), Contribution of the Proinflammatory Cytokine IL-18 in the Formation of Human Nasal Polyps. Anat Rec, 294: 953–960. doi: 10.1002/ar.21385
- Issue published online: 20 MAY 2011
- Article first published online: 28 APR 2011
- Manuscript Accepted: 19 FEB 2011
- Manuscript Received: 6 DEC 2010
- Ministry of Science and Technology of China. Grant Number: 2007AA02Z115
- NSFC. Grant Numbers: 90919032, 30970562
- Specialized Fund for the Doctoral Program of Higher Education. Grant Number: 20091202110001
- Tianjin Educational Committee Foundation. Grant Number: 2008ZD01
- Tianjin Municipal Science and Technology Commission. Grant Numbers: 08ZCGHHZ01900, 08JCYBJC07700
- nasal polyps;
Nasal polyposis is a chronic inflammatory disease of the nasal mucosa. The etiology and the mechanisms of formation of nasal polyps are still not clear. Interleukin (IL)-18 is a novel proinflammatory cytokine that plays important roles in regulating immune inflammatory responses. However, the presence of IL-18 in human nasal mucosa and its roles in the inflammatory process of nasal polyps has not been studied yet. In this study, it was the first time to investigate the expression of IL-18 in human nasal mucosa and nasal polyps, and its potential function in the formation of nasal polyps. Surgical samples were analyzed by Western blot and immunohistochemistry to evaluate the expression and location of IL-18, and its correlated cytokines, IL-4, and IFN-γ. Furthermore, the airway epithelial cell line, A549, was used to investigate the mutual regulation of IFN-γ, IL-4, and IL-18. IFN-γ, IL-4, and IL-18 were all highly expressed in the epithelial cells, submucosal glands, and infiltrating inflammatory cells in the nasal polyp tissues, comparing with the control samples. Especially, the expression of IL-18 was upregulated significantly in nasal polyp tissues compared with control tissues. In addition, IL-18 was expressed in A549 cells in response to lipopolysaccharide and IL-4. Our data suggest that nasal epithelial cells are involved in the pathogenesis of nasal polyps formation and potentially via the secretion of IL-18, which is likely to play important roles in the formation of nasal polyps. Anat Rec, , 2011. © 2011 Wiley-Liss, Inc.