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Relevance of the genetic polymorphism of NOD1 in Chlamydia pneumoniae seropositive stroke patients
Author(s) -
Tiszlavicz Z.,
Somogyvári F.,
Kocsis Á. K.,
Szolnoki Z.,
Sztriha L. K.,
Kis Z.,
Vécsei L.,
Mándi Y.
Publication year - 2009
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2009.02698.x
Subject(s) - nod1 , genotype , chlamydia , medicine , stroke (engine) , chlamydophila pneumoniae , allele , gastroenterology , polymorphism (computer science) , chlamydiaceae , immunology , biology , receptor , gene , genetics , nod2 , mechanical engineering , innate immune system , engineering
Background and purpose: 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. Materials and 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. Conclusion: 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.