title: Low SPINK5 expression in chronic rhinosinusitis.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Otorhinolaryngology, Head and Neck Surgery, University Medical Center, Johannes Gutenberg University Mainz, Mainz, Germany. kai.fruth@unimedizin-mainz.de
authors.forename: Kai
authors.initials: K
authors.lastname: Fruth
authors.forename: Gyula
authors.initials: G
authors.lastname: Goebel
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Koutsimpelas
authors.forename: Jan
authors.initials: J
authors.lastname: Gosepath
authors.forename: Irene
authors.initials: I
authors.lastname: Schmidtmann
authors.forename: Wolf J
authors.initials: WJ
authors.lastname: Mann
authors.forename: Juergen
authors.initials: J
authors.lastname: Brieger
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin; D001249:Asthma / Q000235:genetics / Q000473:pathology; D002908:Chronic Disease; D004342:Drug Hypersensitivity; D005260:Female; D005786:Gene Expression Regulation; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D009297:Nasal Mucosa / Q000378:metabolism / Q000473:pathology; D009298:Nasal Polyps / Q000235:genetics / Q000473:pathology; D016133:Polymerase Chain Reaction / Q000379:methods; D020641:Polymorphism, Single Nucleotide; D053491:Proteinase Inhibitory Proteins, Secretory / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D012016:Reference Values; D012220:Rhinitis / Q000235:genetics* / Q000378:metabolism; D012494:Sampling Studies; D012680:Sensitivity and Specificity; D000074163:Serine Peptidase Inhibitor Kazal-Type 5; D012852:Sinusitis / Q000235:genetics* / Q000378:metabolism; D046509:Tissue Culture Techniques; D055815:Young Adult
chemical_list: D053491:Proteinase Inhibitory Proteins, Secretory; D012333:RNA, Messenger; C120650:SPINK5 protein, human; D000074163:Serine Peptidase Inhibitor Kazal-Type 5; D001241:Aspirin