Edited by: Reto Crameri
A pathway-based approach to find novel markers of local glucocorticoid treatment in intermittent allergic rhinitis
Article first published online: 23 JUL 2010
© 2010 John Wiley & Sons A/S
Volume 66, Issue 1, pages 132–140, January 2011
How to Cite
Wang, H., Chavali, S., Mobini, R., Muraro, A., Barbon, F., Boldrin, D., Åberg, N. and Benson, M. (2011), A pathway-based approach to find novel markers of local glucocorticoid treatment in intermittent allergic rhinitis. Allergy, 66: 132–140. doi: 10.1111/j.1398-9995.2010.02444.x
- Issue published online: 3 DEC 2010
- Article first published online: 23 JUL 2010
- Accepted for publication 14 June 2010
- allergic rhinitis;
- gene expression microarray analysis;
To cite this article: Wang H, Chavali S, Mobini R, Muraro A, Barbon F, Boldrin D, Åberg N, Benson M. A pathway-based approach to find novel markers of local glucocorticoid treatment in intermittent allergic rhinitis. Allergy 2011; 66: 132–140.
Background: Glucocorticoids (GCs) may affect the expression of hundreds of genes in different cells and tissues from patients with intermittent allergic rhinitis (IAR). It is a formidable challenge to understand these complex changes by studying individual genes. In this study, we aimed to identify (i) pathways affected by local GC treatment and (ii) examine if those pathways could be used to find novel markers of local GC treatment in nasal fluids from patients with IAR.
Methods: Gene expression microarray- and iTRAQ-based proteomic analyses of nasal fluids, nasal fluid cells and nasal mucosa from patients with IAR were performed to find pathways enriched for differentially expressed genes and proteins. Proteins representing those pathways were analyzed with ELISA in an independent material of nasal fluids from 23 patients with IAR before and after treatment with a local GC.
Results: Transcriptomal and proteomic high-throughput analyses of nasal fluids, nasal fluid cells and nasal mucosal showed that local GC treatment affected a wide variety of pathways in IAR such as the glucocorticoid receptor pathway and the acute phase response pathway. Extracellular proteins encoded by genes in those pathways were analyzed in an independent material of nasal fluids from patients. Proteins that changed significantly in expression included known biomarkers such as eosinophil cationic protein but also proteins that had not been previously described in IAR, namely CCL2, M-CSF, CXCL6 and apoH.
Conclusion: Pathway-based analyses of genomic and proteomic high-throughput data can be used as a complementary approach to identify novel potential markers of GC treatment in IAR.