1. Epithelial genes in chronic rhinosinusitis with and without nasal polyps.
- Author
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Richer SL, Truong-Tran AQ, Conley DB, Carter R, Vermylen D, Grammer LC, Peters AT, Chandra RK, Harris KE, Kern RC, and Schleimer RP
- Subjects
- Biomarkers, Tumor, Calcium-Binding Proteins biosynthesis, Calgranulin A biosynthesis, Calgranulin A genetics, Chronic Disease, Humans, Immunohistochemistry, Nasal Mucosa metabolism, Nasal Mucosa pathology, Nasal Polyps complications, Nasal Polyps pathology, Phosphoproteins biosynthesis, Phosphoproteins genetics, Polymerase Chain Reaction, Prognosis, Proteinase Inhibitory Proteins, Secretory biosynthesis, Proteinase Inhibitory Proteins, Secretory genetics, Receptors, G-Protein-Coupled biosynthesis, Receptors, G-Protein-Coupled genetics, Rhinitis complications, Rhinitis pathology, S100 Calcium Binding Protein A7, S100 Proteins, Serine Peptidase Inhibitor Kazal-Type 5, Serine Proteinase Inhibitors, Sinusitis complications, Sinusitis pathology, Sodium-Hydrogen Exchangers biosynthesis, Sodium-Hydrogen Exchangers genetics, Calcium-Binding Proteins genetics, Calgranulin B genetics, Gene Expression, Nasal Polyps genetics, RNA, Messenger genetics, Rhinitis genetics, Sinusitis genetics
- Abstract
Background: Genetic studies on chronic inflammatory diseases have resulted in an emphasis on the epithelial interface with the environment and the genes that influence this interaction. This study examines the expression of key epithelial genes implicated in the pathogenesis of other inflammatory disorders for their role in chronic rhinosinusitis (CRS)., Methods: Epithelial cells were collected from the inferior turbinate, middle turbinate, and/or uncinate from 62 subjects undergoing sinonasal surgery. Patient groups included 21 CRS patients with nasal polyposis, 23 CRS patients without nasal polyposis, and 18 controls. Samples were analyzed for S100A7, S100A8, S100A9, SLC9A3R1, G-protein-coupled receptor for asthma, and serine protease inhibitor kazal type 5 (SPINK5) by quantitative real-time polymerase chain reaction. Immunohistochemistry (IHC) was performed to analyze expression of SPINK5 lympho epithelial kazal-type inhibitor (LEKTI) in sinonasal samples., Results: Expression of S100A7 and S100A8 was significantly decreased in CRS with and without nasal polyps when compared with controls. S100A9 expression was significantly decreased in CRS without nasal polyps, and SPINK5 expression was significantly decreased in CRS with nasal polyps. SPINK5 (LEKTI) protein was detected in sinonasal tissue and was significantly decreased in polyp samples using IHC., Conclusion: This study shows marked reductions in the level of expression of several genes involved in epithelial barrier maintenance and repair in the inflammatory state of CRS.
- Published
- 2008
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