title: Relevance of the genetic polymorphism of NOD1 in Chlamydia pneumoniae seropositive stroke patients.
abstract: OBJECTIVE
  Chronic infections with certain pathogens, such as Chlamydia pneumoniae, and genetic parameters that influence inflammatory reactions have been suggested to contribute to ischaemic stroke. NOD1 is a potent cytosolic receptor for C. pneumoniae. The aim of this study was to investigate the genetic polymorphism of NOD1 from the aspect of the development of stroke.
  
  
  METHODS
  A total of 280 patients with ischaemic stroke were enrolled in the study; 150 healthy blood donors served as controls. The G796A (E266K) NOD1 polymorphism was determined by restriction fragment length polymorphism. Chlamydia pneumoniae seropositivity was tested by ELISA.
  
  
  RESULTS
  There was a significant difference in NOD1 G796A genotype distribution between the controls and the stroke patients with C. pneumoniae seropositivity. The AA homozygote and GA heterozygote mutant variants were detected in 16% (25 of 152) and in 50% (77 of 152) of the C. pneumoniae-positive stroke patients, as compared with 8% (6 of 84), and 28% (24 of 84), respectively, in the C. pneumoniae-positive healthy controls. (OR = 2.559; 95% CI = 1.105-6.517, P = 0.04 and OR = 2.567; 95% CI = 1.451-4.540 P < 0.001, respectively). The stroke patients with the large vessel pathology exhibited the highest frequency of the mutant allele A (51%). In contrast, amongst the C. pneumoniae-negative subjects, no difference in genotype frequency was observed between the stroke patients and the controls.
  
  
  CONCLUSIONS
  Polymorphism in NOD1 G796A alone did not prove to be a risk factor for stroke in general, but in association with C. pneumoniae infection it appeared to be accompanied by an increased risk of the development of stroke.
authors.affiliation: Department of Medical Microbiology and Immunobiology, University of Szeged, Szeged, Hungary.
authors.forename: Z
authors.initials: Z
authors.lastname: Tiszlavicz
authors.forename: F
authors.initials: F
authors.lastname: Somogyvári
authors.forename: A K
authors.initials: AK
authors.lastname: Kocsis
authors.forename: Z
authors.initials: Z
authors.lastname: Szolnoki
authors.forename: L K
authors.initials: LK
authors.lastname: Sztriha
authors.forename: Z
authors.initials: Z
authors.lastname: Kis
authors.forename: L
authors.initials: L
authors.lastname: Vécsei
authors.forename: Y
authors.initials: Y
authors.lastname: Mándi
mesh_terms: D000368:Aged; D000483:Alleles; D054458:Amplified Fragment Length Polymorphism Analysis; D016009:Chi-Square Distribution; D023521:Chlamydophila Infections / Q000150:complications* / Q000235:genetics; D016993:Chlamydophila pneumoniae / Q000235:genetics; D002908:Chronic Disease; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D053474:Nod1 Signaling Adaptor Protein / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D020521:Stroke / Q000150:complications* / Q000235:genetics
chemical_list: C119067:NOD1 protein, human; D053474:Nod1 Signaling Adaptor Protein