This study was approved by the institutional review board and performed in accordance to the actual version of the declaration of Helsinki.
Article first published online: 8 MAY 2012
Copyright © 2012 The American Laryngological, Rhinological, and Otological Society, Inc.
Volume 122, Issue 6, pages 1198–1204, June 2012
How to Cite
Fruth, K., Goebel, G., Koutsimpelas, D., Gosepath, J., Schmidtmann, I., Mann, W. J. and Brieger, J. (2012), Low SPINK5 expression in chronic rhinosinusitis. The Laryngoscope, 122: 1198–1204. doi: 10.1002/lary.23300
The authors have no funding, financial relationships, or conflicts of interest to disclose.
- Issue published online: 1 JUN 2012
- Article first published online: 8 MAY 2012
- Accepted manuscript online: 22 MAR 2012 10:19AM EST
- Manuscript Accepted: 22 FEB 2012
- Manuscript Revised: 16 FEB 2012
- Manuscript Received: 17 OCT 2011
- Chronic rhinosinusitis;
- nasal polyps;
- aspirin intolerance;
- Samter triad;
- Level of Evidence: 2b
Chronic rhinosinusitis (CRS) is a multifactorial disease that probably arises as a result of genetic diversity and environmental factors. SPINK5 is a serine protease inhibitor, which is supposed to be an important regulator of epithelial barrier maintenance. The role of SPINK5 polymorphisms and expression in CRS, especially in individuals with aspirin intolerance, is unclear.
SPINK5 single-nucleotide polymorphisms (SNPs) and SPINK5 expression levels were correlated with CRS without (CRSsNP) and with nasal polyps (CRSwNP), aspirin intolerance, asthma, and allergies.
One hundred four nasal tissue samples, 15 from patients with CRSsNP, 59 from patients with CRSwNP, and 30 from healthy controls of the inferior turbinate, were analyzed for their SPINK5 status. Genotypes of four SPINK5 single nucleotide polymorphism (SNPs; G1258A, G2475T, A2915G, and A1103G), as well as SPINK5 mRNA expression levels, were determined by polymerase chain reaction.
No correlation between any SPINK5 SNP and CRSsNP, CRSwNP, or allergies and asthma was observed. The heterozygous SNPs G1258A and A1103G were observed more frequently in aspirin-intolerant patients; the homozygous (A/A) genotype of SNP 1258 and the homozygous (G/G) genotype SNP 1103 were less frequent. There was no correlation between the analyzed SNPs and the level of SPINK5 expression. It was noted that in individuals with CRSwNP, aspirin intolerance, and allergies, SPINK5 expression was lowered.
G1258A and A1103G polymorphisms are distinctive for the aspirin intolerance syndrome. Lowered SPINK5 expression might be a contributing factor leading to CRS, and appears to be characteristic for patients suffering from aspirin intolerance and from allergies. Laryngoscope, 2012