title: Common CCR 5 polymorphism in stroke: the CCR 5 delta32 polymorphism differentiates cardioembolism from other aetiologies of ischaemic cerebrovascular diseases.
abstract: Inflammation is involved in the development of atherosclerosis. The CC chemokine receptor 5 (CCR5) initiates chemotaxis and modulates the inflammation secondary to atherosclerosis and related vascular diseases. The CCR5 Delta32 polymorphism influences the expression of CCR5 on the cell surface. The purpose of this study was to examine the effect of the Delta32 polymorphism in ischaemic cerebrovascular disease (ICVD). The CCR5 Delta32 polymorphism was genotyped in 1462 individuals: 562 ischaemic stroke (IS), 97 transient ischaemic attack (TIA) and in 803 healthy controls. All 659 ICVD patients were categorized according to the Trial of Org 10172 in Acute Stroke Treatment aetiological classification. The investigated subtypes were large artery atherosclerosis (LAA), cardioembolism (CE), small artery occlusion (SAO) and cryptogenic disease (CRYPT). Genotyping was performed with the TaqMan polymerase chain reaction. The Delta32 allele was less frequent in CE patients compared with LAA (OR, 0.4; 95% CI, 0.24-0.79; P = 0.008), SAO (OR, 0.5; 95% CI, 0.29-0.84; P = 0.01), CRYPT (OR, 0.5; 95% CI, 0.28-0.82; P = 0.008) and controls (OR, 0.5; 95% CI, 0.36-0.82; P = 0.002). Multiple logistic regression analysis showed that the Delta32 allele is associated with a lower risk for cardioembolic ICVD (OR 0.5; 95% CI, 0.28-0.75; P = 0.002) when compared with ICVD of other causes. The Delta32 polymorphism of CCR5 may differentiate cardioembolism from the remaining causes of ICVD.
authors.affiliation: Department of Neurology, Neuro-Angiological Research Center, Karolinska Institutet at Karolinska University Hospital, Huddinge, Sweden. Nikolaos.Kostulas@ki.se
authors.forename: N
authors.initials: N
authors.lastname: Kostulas
authors.forename: K
authors.initials: K
authors.lastname: Nikolaos
authors.forename: I
authors.initials: I
authors.lastname: Markaki
authors.forename: M
authors.initials: M
authors.lastname: Ioanna
authors.forename: V
authors.initials: V
authors.lastname: Kostulas
authors.forename: K
authors.initials: K
authors.lastname: Vasilios
authors.forename: J
authors.initials: J
authors.lastname: Hillert
authors.forename: H
authors.initials: H
authors.lastname: Jan
authors.forename: K
authors.initials: K
authors.lastname: Kostulas
authors.forename: K
authors.initials: K
authors.lastname: Konstantinos
mesh_terms: D000368:Aged; D001157:Arterial Occlusive Diseases / Q000150:complications / Q000235:genetics; D050197:Atherosclerosis / Q000150:complications / Q000235:genetics; D002545:Brain Ischemia / Q000235:genetics; D002340:Carotid Artery Diseases / Q000150:complications / Q000235:genetics; D004617:Embolism / Q000150:complications*; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D002546:Ischemic Attack, Transient / Q000235:genetics; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D019713:Receptors, CCR5 / Q000235:genetics*; D012307:Risk Factors; D020521:Stroke / Q000209:etiology*
chemical_list: D019713:Receptors, CCR5