Increased cytokine release by leucocytes in survivors of stroke at young age

Eur J Clin Invest. 2001 Nov;31(11):999-1006. doi: 10.1046/j.1365-2362.2001.00923.x.

Abstract

Background: Enhanced stimulus-induced release of pro-inflammatory cytokines by leucocytes may contribute to the pathogenesis of ischaemic stroke.

Design: We investigated the lipopolysaccharide-induced release of interleukin-1beta (IL-1beta), IL-6, IL-8, and tumour necrosis factor-alpha (TNF-alpha) 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.

Results: Release of IL-8 was higher (P = 0.006) and release of TNF-alpha 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.

Conclusions: We conclude that high inducible release of IL-8--and possibly of TNF-alpha and IL-6--may contribute to the odds of ischaemic stroke in young adults.

MeSH terms

  • Adult
  • Aging
  • Aortic Dissection / immunology
  • Female
  • Humans
  • Interleukin-1 / genetics
  • Interleukin-1 / metabolism*
  • Interleukin-6 / metabolism*
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism*
  • Leukocytes / immunology*
  • Leukocytes / metabolism
  • Lipopolysaccharides / pharmacology
  • Male
  • Polymorphism, Genetic
  • Risk Factors
  • Stroke / immunology*
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Interleukin-1
  • Interleukin-6
  • Interleukin-8
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha