Gene and protein expression of protease-activated receptor 2 in structural and inflammatory cells in the nasal mucosa in seasonal allergic rhinitis

Summary Background Protease‐activated receptor 2 (PAR 2) has been shown to be responsible for trypsin and mast cell tryptase‐induced airway inflammation. Here, the present study aimed to explore the expression of PAR 2 in the nasal mucosa of seasonal allergic rhinitis (SAR). Methods Study subjects w...

Full description

Saved in:

Bibliographic Details
Published in:	Clinical and experimental allergy Vol. 36; no. 8; pp. 1039 - 1048
Main Authors:	Dinh, Q. T., Cryer, A., Trevisani, M., Dinh, S., Wu, S., Cifuentes, L. B., Feleszko, W. K., Williams, A., Geppetti, P., Fan Chung, K., Heppt, W., Klapp, B. F., Fischer, A.
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-08-2006 Blackwell
Subjects:	Adolescent Adult Allergic diseases Biological and medical sciences Case-Control Studies Eosinophils - chemistry Epithelial Cells - chemistry Epithelial Cells - immunology Female Fundamental and applied biological sciences. Psychology Fundamental immunology Gene Expression human nasal mucosa Humans Immunohistochemistry - methods Immunopathology Leukocyte Count Male Mast Cells - chemistry Medical sciences Middle Aged Nasal Mucosa - chemistry Nasal Mucosa - immunology non-allergic rhinitis (NR) perennial allergic rhinitis protease-activated receptor 2 (PAR 2) Receptor, PAR-2 - analysis Receptor, PAR-2 - genetics Reverse Transcriptase Polymerase Chain Reaction Rhinitis, Allergic, Seasonal - immunology Rhinitis, Allergic, Seasonal - metabolism seasonal allergic rhinitis (SAR) Taqman Allergy Nose disease Rhinitis Mucosa PAR2 protease-activated receptor perennial allergic rhinitis human nasal mucosa Immunology ENT disease non-allergic rhinitis (NR) Human Immunopathology Lung disease Respiratory disease Inflammation Gene expression Protein Infection Polymerase chain reaction Taqman protease-activated receptor 2 (PAR 2) Viral disease seasonal allergic rhinitis (SAR) Technique Molecular biology
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Summary Background Protease‐activated receptor 2 (PAR 2) has been shown to be responsible for trypsin and mast cell tryptase‐induced airway inflammation. Here, the present study aimed to explore the expression of PAR 2 in the nasal mucosa of seasonal allergic rhinitis (SAR). Methods Study subjects were recruited for the study by medical history, physical examination and laboratory screening tests. Using immunohistochemistry, laser‐assisted cell picking and subsequently real‐time PCR, nasal mucosa biopsies of SAR patients were investigated for PAR 2 gene and protein expression in complex tissues of the nasal mucosa. Results Gene and protein expression of PAR 2 was firstly detected in nasal mucosa of SAR patients. The relative gene expression level of PAR 2 was significantly increased in complex tissues of the nasal mucosa of SAR (6.21±4.02 vs. controls: 1.38±0.86, P=0.004). Moreover, PAR 2 mRNA expression in epithelial cells (SAR: 4.78±4.64 vs. controls: 0.84±0.61, P=0.003) but not in mucus (SAR: 1.51±1.15 vs. controls: 1.35±1.02, P=0.78) and endothelial cells (SAR: 1.20±0.57 vs. controls: 1.73±1.30, P=0.5) was found to be significantly changed in the nasal mucosa in SAR. Using double immunohistochemistry the present study demonstrated that the total numbers of mast cells (P=0.0003) and eosinophils (P=0.03) and the numbers of eosinophils expressing PAR 2 (P=0.006) were significantly elevated in the nasal mucosa of SAR compared with the controls. Conclusion The abundant presence and distribution of gene and protein expression of PAR 2 in different cell types in the nasal mucosa under normal situation, the increased expression of PAR 2 in epithelial cells and the increased number of eosinophils with PAR 2 suggest that PAR 2 may contribute to the pathogenesis of allergic diseases such as SAR.
Bibliography:	ark:/67375/WNG-H59G76BM-K istex:43D7C005CE3C645698CD3C1C1E2C2EA594C4A1F1 ArticleID:CEA2537 1 These authors contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0954-7894 1365-2222
DOI:	10.1111/j.1365-2222.2006.02537.x