Both the authors contributed equally to this article.
Clara cell 10-kDa protein expression in chronic rhinosinusitis and its cytokine-driven regulation in sinonasal mucosa
Article first published online: 12 DEC 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Munksgaard
Volume 64, Issue 1, pages 149–157, January 2009
How to Cite
Liu, Z., Lu, X., Zhang, X. H., Bochner, B. S., Long, X. B., Zhang, F., Wang, H. and Cui, Y. H. (2009), Clara cell 10-kDa protein expression in chronic rhinosinusitis and its cytokine-driven regulation in sinonasal mucosa. Allergy, 64: 149–157. doi: 10.1111/j.1398-9995.2008.01847.x
- Issue published online: 23 DEC 2008
- Article first published online: 12 DEC 2008
- Accepted for publication 12 June 2008
- chronic rhinosinusitis;
- clara cell 10-kDa protein;
- nasal polyps;
Background: Clara cell 10-kDa protein (CC10) is a multifunction protein with anti-inflammatory and immunomodulatory effects; hence we compared the CC10 expression between chronic rhinosinusitis (CRS) patients with and without nasal polyps (NPs), analyzed its association with disease severity and response to surgery, and explored its regulation via cytokines.
Methods: The plasma and tissue CC10 levels were compared between controls and CRS patients with and without NPs by means of quantitative RT-PCR, ELISA, and immunohistochemistry. Computed tomography (CT) scan and endoscopy findings and symptoms were scored. Nasal explant culture was used to explore the effect of TNF-α, IL-1β, IL-4, INF-γ, and IL-10 on CC10 gene regulation.
Results: Compared with controls, the CC10 expression in sinonasal mucosa was significantly inhibited in both CRS patients with and without NPs. There was a significant further decrease of CC10 expression in patients with NPs and asthma. No difference in CC10 plasma levels was found between controls and patients. CC10 levels inversely correlated with preoperative CT scores, and postoperative endoscopy and symptom scores. TNF-α, IL-1β and IL-4 inhibited, whereas INF-γ and IL-10 promoted CC10 production in nasal mucosa. A significantly faster decay of CC10 transcripts was seen after IL-1β treatment. IL-1β and IL-10 induced thyroid transcription factor-1 expression. INF-γ increased, whereas IL-4 inhibited hepatocyte nuclear factor-3α expression.
Conclusion: CC10 may take part in the pathogenesis of CRS and correlates with disease severity and response to surgery. Different cytokines can regulate CC10 expression in nasal mucosa differentially through modulating mRNA stability and certain transcriptional factors expression.