title: Polymorphism in the promoter of lipopolysaccharide receptor CD14 and ischemic cerebrovascular disease.
abstract: OBJECTIVE
  A growing amount of evidence suggests that infectious and inflammatory processes may be involved in the initiation of arteriosclerosis, but the mechanisms are conceivably multifactorial and complex. Two European groups have recently demonstrated that a C(-260)-->T polymorphism in the promoter of the CD14 lipopolysaccharide receptor may be a risk factor for coronary artery disease (CAD). The T allele of this polymorphism reportedly increases the expression of CD14 and may be involved in atherogenesis. In the present study we investigated a possible association between the C(-260)-->T polymorphism in the CD14 promoter and the occurrence of symptomatic ischemic cerebrovascular disease (CVD).
  
  
  METHODS
  Genotype frequencies of the C(-260)-->T polymorphism in the CD14 promoter were determined in 235 patients with CVD, as confirmed by brain CT and/or MRI, and 309 age- and sex-matched control subjects.
  
  
  RESULTS
  The distribution of genotypes was as follows: CVD patients, T:/T: 24.3%, C:/T: 53.2%, and C:/C: 22. 6%; controls, T:/T: 26.9%, C:/T: 50.2%, and C:/C: 23.0%. There was no significant difference between the CD14 promoter genotypes of the CVD patients and the controls (chi(2)=0.601, P:=0.741). We also measured the concentration of serum soluble CD14 and the density of membranous CD14 on monocytes in the CVD patients, but the polymorphism was not associated with either the concentration of soluble CD14 or the density of membranous CD14 (P:=0.358, P:=0.238, respectively).
  
  
  CONCLUSIONS
  Our results indicate that the C(-260)-->T polymorphism in the CD14 promoter is not associated with an increased risk for CVD.
authors.affiliation: Department of Neurology, School of Medicine, Keio University, Tokyo, Japan.
authors.forename: D
authors.initials: D
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Murata
authors.forename: N
authors.initials: N
authors.lastname: Tanahashi
authors.forename: H
authors.initials: H
authors.lastname: Sato
authors.forename: A
authors.initials: A
authors.lastname: Sonoda
authors.forename: I
authors.initials: I
authors.lastname: Saito
authors.forename: K
authors.initials: K
authors.lastname: Watanabe
authors.forename: Y
authors.initials: Y
authors.lastname: Fukuuchi
mesh_terms: D002561:Cerebrovascular Disorders / Q000175:diagnosis* / Q000453:epidemiology / Q000235:genetics; D005260:Female; D006801:Humans; D007564:Japan / Q000453:epidemiology; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012307:Risk Factors
chemical_list: D018950:Lipopolysaccharide Receptors