1These authors contributed equally to this work.
Transcriptional up-regulation of histamine receptor-1 in epithelial, mucus and inflammatory cells in perennial allergic rhinitis
Article first published online: 9 NOV 2005
Clinical & Experimental Allergy
Volume 35, Issue 11, pages 1443–1448, November 2005
How to Cite
Dinh, Q. T. , Cryer, A., Dinh, S., Peiser, C., Wu, S., Springer, J., Hamelmann, E., Klapp, B. F., Heppt, W. and Fischer, A. (2005), Transcriptional up-regulation of histamine receptor-1 in epithelial, mucus and inflammatory cells in perennial allergic rhinitis. Clinical & Experimental Allergy, 35: 1443–1448. doi: 10.1111/j.1365-2222.2005.02359.x
- Issue published online: 9 NOV 2005
- Article first published online: 9 NOV 2005
- Submitted 23 December 2004; revised 24 August 2005; accepted 31 August 2005
- histamine receptor 1;
- human nasal mucosa;
- laser-assisted microdissection;
- perennial allergic rhinitis (PAR);
Background Histamine receptors play an important role in the pathogenesis of nasal allergy. Activation of histamine receptor 1 (H1R) and 2 (H2R) can cause allergic symptoms which can be blocked effectively by antihistamines. H1R and H2R transcript levels have been found to be up-regulated in perennial – but not in seasonal – allergic rhinitis (AR). The present study aimed to explore H1R and H2R expression in complex tissues of the nasal mucosa of perennial allergic rhinitis (PAR).
Methods Ten patients with PAR and 13 non-AR subjects were recruited for the study by medical history, physical examination and laboratory screening tests. In this study, we have analysed single cells dissected from the nasal mucosa biopsies by laser-assisted microdissection. H1R mRNA expression was analysed in different cell types such as epithelial, endothelial, mucus and inflammatory cells isolated from the nasal mucosa of PAR in comparison with non-AR subjects.
Results H1R mRNA gene expression level was significantly increased in the nasal mucosa of PAR in comparison with non-AR (P<0.0001). H1R mRNA was significantly elevated in epithelial (P<0.001) and mucus cells (P<0.05) of PAR in comparison with non-AR whereas H1R gene expression levels in endothelial cells between both groups were not changed (P=0.23). Interestingly, inflammatory cells in the nasal mucosa of PAR patients were also strongly expressed H1R mRNA (P<0.001).
Conclusion The present study indicates that PAR alters the expression of H1R mRNA in epithelial, mucus and inflammatory cells of the nasal mucosa and but not in endothelial cells. Therefore, epithelial, mucus and inflammatory cells may play an important role in histamine-mediated allergic airway inflammation in PAR.