[Cytokines in clinical and experimental ischemic stroke].

Inflammatory reaction following acute cerebral ischaemia exacerbates infarct size and neurological deficit. Brain resident cells localised within ischaemic region rapidly synthesise cytokines, proteins involved in cellular communication. The cytokines become important mediators of endothelial-leukocyte interactions leading to the influx of haematogenous inflammatory cells into the brain ischaemic region. Proinflammatory cytokines: tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) initiate inflammatory reaction and induce expression of other cytokines and inflammatory mediators. The presence of cytokines in brain infarct region has been shown in human and animal autopsy studies. Suppression of proinflammatory cytokines expression reduces brain infarct size in animal models of stroke. Increased levels of proinflammatory cytokines in cerebrospinal fluid and/or in serum of acute ischaemic stroke patients correlate with brain infarct volume and stroke severity and may have a predictive value for stroke outcome. This review presents cytokines studied in clinical and experimental strokes documenting that the molecules may exert not only detrimental but also neuroprotective effect on ischaemic brain.