eISSN: 1896-9151
ISSN: 1734-1922
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vol. 5

Cell adhesion molecular markers in ischaemic stroke patients: correlation with clinical outcome and comparison with primary autoimmune disease

Edyta Matusik
Andrzej Wajgt
Joanna Janowska
Barbara Zahorska-Markiewicz
Bernhard Schaller
Elżbieta Zych-Twardowska

Arch Med Sci 2009; 5, 2: 182-189
Online publish date: 2009/07/23
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Both humoral and cellular secondary inflammation form an inseparable process, which accompanies acute ischaemic stroke [1-3] with evidence that these responses may exacerbate tissue injury. Acute cerebral ischaemia followed by reperfusion therefore leads violently to the activation of proinflammatory cytokine production by the immunological cells which infiltrate the ischaemic core in the early and late phase of the process and which stimulate endothelial cells, neurons, astrocytes and microglia cells as well [4]. A secondary inflammatory or immunological response includes the increased expression of the cell adhesion molecules that play a very significant and critical role in both normal and in various pathophysiological disease states. The crucial role for this inflammation response after ischaemic stroke is in the leukocytes’ adhesion to endothelial cells and their migration through the blood-brain barrier [4-6]. This inflammation response during cerebral ischaemia, through activation of endothelial cells, leads to excretion of soluble forms of cell adhesion molecules such as ICAM-1 (intercellular adhesion molecule-1) or VCAM-1 (vascular cell adhesion molecule-1) into the bloodstream [4-6]. These inflammatory cells can then move through the endothelium by diapedesis and release cytokines and enzymes that are important components in the progression of the ischaemic lesion. The profiles of soluble forms of these cell adhesion molecules in the serum, and their role during cerebral ischaemia, have not yet been defined in detail. It is also not understood whether there exists a correlation between the soluble forms of cell adhesion molecules and the neurological outcome in ischaemic stroke patients, but this may be interesting because we still need to find new prognostic factors and therapeutic targets in ischaemic stroke. The existing few data are therefore often conflicting [7-10], as some authors have provided evidence that members of the soluble cell adhesion molecules superfamily may be linked with the clinical outcome [7-9], like other inflammatory components in ischaemic stroke [11, 12]. But others have shown that soluble forms of cell adhesion molecules have no or very weak objective predictive value in the assessment of stroke patients [10]. It seems to be also very interesting to know the severity of this secondary immune response. The most valuable reference group on that point is the group of multiple...

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