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Systemic complement activation following human acute ischaemic stroke.

E D Pedersen1, U Waje-Andreassen, C A Vedeler

  • 1Institute of Immunology, Rikshospitalet University Hospital, Oslo, Norway. e.d.pedersen@labmed.uio.no

Clinical and Experimental Immunology
|June 16, 2004
PubMed
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Systemic complement activation occurs transiently after stroke. C-reactive protein (CRP) rises early, followed by terminal complement complex (TCC) increase, suggesting CRP may activate complement, contributing to stroke inflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Stroke-induced brain damage involves inflammation, with the complement system playing a key role.
  • Ischaemia-reperfusion injury is a significant factor in post-stroke inflammation.

Purpose of the Study:

  • To investigate systemic complement activation after acute ischaemic stroke.
  • To examine the relationship between complement activation, C-reactive protein (CRP), and other inflammatory mediators.

Main Methods:

  • Plasma samples from 11 acute stroke patients and 9 healthy controls were analyzed over 12 months.
  • Measurements included terminal SC5b-9 complement complex (TCC), CRP, soluble adhesion molecules, and cytokines.

Main Results:

Related Experiment Videos

  • Terminal complement complex (TCC) and CRP levels increased significantly post-stroke, peaking within the first week and then normalizing.
  • Both TCC and CRP elevations correlated with the size of the infarction.
  • No significant changes were observed in adhesion molecules or cytokines.

    • Conclusions:

    • A transient systemic complement activation occurs following acute ischaemic stroke.
    • The early rise in CRP followed by TCC increase suggests CRP may activate the complement system, contributing to post-stroke inflammation.