Epithelial genes in chronic rhinosinusitis with and without nasal polyps.
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.


CONCLUSIONS
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.
Richer
Sara L
SL
Department of Otolaryngology-Head and Neck Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA. sara.richer@gmail.com
Truong-Tran
Ai Q
AQ
Conley
David B
DB
Carter
Roderick
R
Vermylen
David
D
Grammer
Leslie C
LC
Peters
Anju T
AT
Chandra
Rakesh K
RK
Harris
Kathleen E
KE
Kern
Robert C
RC
Schleimer
Robert P
RP
D014408:Biomarkers, Tumor; D002135:Calcium-Binding Proteins / Q000096:biosynthesis / Q000235:genetics*; D040501:Calgranulin A / Q000096:biosynthesis / Q000235:genetics; D040502:Calgranulin B / Q000235:genetics*; D002908:Chronic Disease; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D009297:Nasal Mucosa / Q000378:metabolism / Q000473:pathology; D009298:Nasal Polyps / Q000150:complications / Q000235:genetics* / Q000473:pathology; D010750:Phosphoproteins / Q000096:biosynthesis / Q000235:genetics; D016133:Polymerase Chain Reaction; D011379:Prognosis; D053491:Proteinase Inhibitory Proteins, Secretory / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics*; D043562:Receptors, G-Protein-Coupled / Q000096:biosynthesis / Q000235:genetics; D012220:Rhinitis / Q000150:complications / Q000235:genetics* / Q000473:pathology; D000075023:S100 Calcium Binding Protein A7; D009418:S100 Proteins; D000074163:Serine Peptidase Inhibitor Kazal-Type 5; D015842:Serine Proteinase Inhibitors; D012852:Sinusitis / Q000150:complications / Q000235:genetics* / Q000473:pathology; D017923:Sodium-Hydrogen Exchangers / Q000096:biosynthesis / Q000235:genetics
D014408:Biomarkers, Tumor; D002135:Calcium-Binding Proteins; D040501:Calgranulin A; D040502:Calgranulin B; C484532:NPSR1 protein, human; D010750:Phosphoproteins; D053491:Proteinase Inhibitory Proteins, Secretory; D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; D000075023:S100 Calcium Binding Protein A7; D009418:S100 Proteins; C089242:S100A7 protein, human; C120650:SPINK5 protein, human; D000074163:Serine Peptidase Inhibitor Kazal-Type 5; D015842:Serine Proteinase Inhibitors; D017923:Sodium-Hydrogen Exchangers; C093376:sodium-hydrogen exchanger regulatory factor