Spatial expression of two anti-inflammatory mediators, annexin 1 and galectin-1, in nasal polyposis
Article first published online: 2 OCT 2006
Clinical & Experimental Allergy
Volume 36, Issue 10, pages 1260–1267, October 2006
How to Cite
Sena, A. A. S., Provazzi, P. J. S., Fernandes, A. M., Cury, P. M., Rahal, P. and Oliani, S. M. (2006), Spatial expression of two anti-inflammatory mediators, annexin 1 and galectin-1, in nasal polyposis. Clinical & Experimental Allergy, 36: 1260–1267. doi: 10.1111/j.1365-2222.2006.02570.x
- Issue published online: 2 OCT 2006
- Article first published online: 2 OCT 2006
- Submitted 13 November 2005; revised 22 June 2006; accepted 25 July 2006
- annexin 1;
- epithelial cells;
- inflammatory cells;
- nasal polyp
Background There is renewed interest in the role played by specific counter-regulatory mechanisms to control the inflammatory host response, poorly investigated in human pathology. Here, we monitored the expression of two anti-inflammatory mediators, annexin 1 and galectin-1, and assessed their potential link to glucocorticoids' (GCs) effective control of nasal polyposis (NP).
Methods Total patterns of mRNA and protein expression were analysed by quantitative real-time PCR (qPCR) and Western blotting analyses, whereas ultrastructural immunocytochemistry was used for spatial localization and quantification of each mediator, focusing on mast cells, eosinophils and epithelial cells.
Results Up-regulation of the annexin 1 gene, and down-regulation of galectin-1 gene, was detected in polypoid tissue compared with nasal mucosa. Patient treatment with betamethasone augmented galectin-1 protein expression in polyps. At the cellular level, control mast cells and eosinophils displayed higher annexin 1 expression, whereas marked galectin-1 immunolabelling was detected in the granule matrix of mast cells. Cells of glandular duct epithelium also displayed expression of both annexin 1 and galectin-1, augmented after treatment.
Conclusion Mast cells and epithelial cells appeared to be pivotal cell types involved in the expression of both annexin 1 and galectin-1. It is possible that annexin 1 and galectin-1 could be functionally associated with a specific mechanism in NP and that GC exert at least part of their beneficial effects on the airway mucosa by up-regulating, in a specific cell target fashion, these anti-inflammatory agonists.