title: Effects of interleukin-1 gene polymorphisms on the development of coronary artery disease associated with Chlamydia pneumoniae infection.
abstract: OBJECTIVE
  This study was done to elucidate the effects of interleukin (IL)-1 gene polymorphisms on coronary artery disease (CAD) associated with Chlamydia pneumoniae (CP) infection.
  
  
  BACKGROUND
  It was suggested that CP was associated with CAD. However, genetic factors involved in CAD associated with CP infection are unknown.
  
  
  METHODS
  We evaluated CP immunoglobulin G (IgG) seropositivity and IL-1 beta (a C/T transition at -511) and IL-1 receptor antagonist (IL-1Ra) (a variable-number repeat in intron 2) gene polymorphisms in 292 patients undergoing coronary angiography.
  
  
  RESULTS
  Seropositivity for CP was present in 61% of patients with CAD versus 51% without CAD (p = NS). The percentage of patients having IL-1 beta (-511) C/C genotype and/or IL-1Ra (intron 2) 2- or 3-repeat allele was higher in patients with CAD than without CAD (29 vs. 16%, p < 0.025). To clarify the effects of these CAD-associated variants (IL-1 beta C/C and/or IL-1Ra 2- or 3-repeat), patients were divided into four groups. A stepwise increase in CAD prevalence was observed depending on CP seropositivity and the variants. Odds ratios (ORs) for CAD were 1.4 in the group with seropositivity alone, 1.7 with the variants alone and 3.8 with seropositivity and the variants. Such variants were associated with CAD in both patients with and without seropositivity. Interestingly, high prevalence of myocardial infarction (MI) was confined to the group with seropositivity and the variants (OR, 2.8). The variants were associated with MI only in patients with CP seropositivity.
  
  
  CONCLUSIONS
  The IL-1 gene polymorphisms were found to play a role in the development of CAD, especially MI, in patients with CP infection.
authors.affiliation: First Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan. momiyama@me.ndmc.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Momiyama
authors.forename: R
authors.initials: R
authors.lastname: Hirano
authors.forename: H
authors.initials: H
authors.lastname: Taniguchi
authors.forename: H
authors.initials: H
authors.lastname: Nakamura
authors.forename: F
authors.initials: F
authors.lastname: Ohsuzu
mesh_terms: D000368:Aged; D023521:Chlamydophila Infections / Q000150:complications*; D016993:Chlamydophila pneumoniae; D003327:Coronary Disease / Q000235:genetics* / Q000382:microbiology*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics / Q000382:microbiology; D011110:Polymorphism, Genetic; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*
chemical_list: D007375:Interleukin-1; D017472:Receptors, Interleukin-1