title: Association between the functional polymorphism C-159T in the CD14 promoter gene and nasal polyposis: potential role in asthma.
abstract: BACKGROUND
  Nasal polyposis (NP) is a chronic inflammatory disease that is frequently associated with allergy and asthma. Corticosteroid therapy and surgical removal of polyps are the 2 most common treatment strategies for NP. Various allergic and inflammatory mediators are thought to play a major role in the pathophysiology of this disorder. The CD14 gene is located on chromosome 5q31-32, which is considered a critical region for several allergic and atopic diseases, including asthma. Consequently, variations in CD14 could have functional effects on the etiology and severity of allergy and asthma. The aim of this study was to investigate the association between the polymorphism C-159T in the CD14 gene of patients with NP and controls.
  
  
  METHODS
  The study population comprised 106 patients with NP diagnosed based on computed tomography scan of the paranasal sinus, endoscopy, and histological examination. Findings were compared with those from 87 controls. The frequency of C-159T was determined using polymerase chain reaction-restriction fragment length polymorphism analysis. DNA was extracted using the salting out technique.
  
  
  RESULTS
  A significant association was observed between C-159T and NP (P = .04). Patients with the CC genotype at position -159 of the CD14 promoter region had an increased risk of asthma (OR, 3.83, 95% CI, 0.99-13.91; P < .02). However, we did not find an association between the distribution of C-159T and serum immunoglobulin E level.
  
  
  CONCLUSIONS
  A genetic variation in the CD14 promoter might play a role in the pathogenesis of NP and in the incidence of asthma.
authors.affiliation: Otorhinolaryngology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: N
authors.initials: N
authors.lastname: Yazdani
authors.forename: M M
authors.initials: MM
authors.lastname: Amoli
authors.forename: M
authors.initials: M
authors.lastname: Naraghi
authors.forename: A
authors.initials: A
authors.lastname: Mersaghian
authors.forename: F
authors.initials: F
authors.lastname: Firouzi
authors.forename: F
authors.initials: F
authors.lastname: Sayyahpour
authors.forename: Z
authors.initials: Z
authors.lastname: Mokhtari
mesh_terms: D000328:Adult; D001249:Asthma / Q000453:epidemiology* / Q000235:genetics* / Q000276:immunology; D002895:Chromosomes, Human, Pair 5 / Q000276:immunology; D005260:Female; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D007073:Immunoglobulin E / Q000097:blood; D018836:Inflammation Mediators / Q000276:immunology; D007492:Iran; D018950:Lipopolysaccharide Receptors / Q000235:genetics* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics; D009298:Nasal Polyps / Q000453:epidemiology* / Q000235:genetics* / Q000276:immunology; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics
chemical_list: D018836:Inflammation Mediators; D018950:Lipopolysaccharide Receptors; D007073:Immunoglobulin E