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Increased cytokine release by leucocytes in survivors of stroke at young age
Author(s) -
Grau A. J.,
Aulmann M.,
Lichy C.,
Meiser H.,
Buggle F.,
Brandt T.,
GrondGinsbach C.
Publication year - 2001
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2001.00923.x
Subject(s) - medicine , cytokine , pathogenesis , stroke (engine) , tumor necrosis factor alpha , immunology , interleukin 6 , myocardial infarction , receptor , mechanical engineering , engineering
Enhanced stimulus‐induced release of pro‐inflammatory cytokines by leucocytes may contribute to the pathogenesis of ischaemic stroke. We investigated the lipopolysaccharide‐induced release of interleukin‐1β (IL‐1β), IL‐6, IL‐8, and tumour necrosis factor‐α (TNF‐α) in whole blood from 20 patients with a history of ischaemic stroke under the age of 50, 20 patients with a history of cervical artery dissection (CAD) and 21 age‐ and sex‐matched healthy control subjects. Release of IL‐8 was higher ( P = 0·006) and release of TNF‐α and IL‐6 tended to be higher ( P < 0·1) in young stroke patients than in control subjects. No increased release existed in CAD patients. Vascular risk factors or history of infection before stroke did not modify IL‐8 production. A common T(250) → A polymorphism in the IL‐8 gene promotor was newly identified but did not correlate with the variability of IL‐8 release. The C(260) → T polymorphism in the gene of the monocytic LPS‐receptor CD14 – a risk factor for myocardial infarction – was not associated with increased cytokine release. We conclude that high inducible release of IL‐8 – and possibly of TNF‐α and IL‐6 – may contribute to the odds of ischaemic stroke in young adults.