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Interleukin-1α expression precedes IL-1β after ischemic brain injury and is localised to areas of focal neuronal loss and penumbral tissues
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نویسنده
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luheshi n.m. ,kovács k.j. ,lopez-castejon g. ,brough d. ,denes a.
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منبع
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journal of neuroinflammation - 2011 - دوره : 8 - شماره : 0
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چکیده
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Background: cerebral ischemia is a devastating condition in which the outcome is heavily influenced by inflammatory processes,which can augment primary injury caused by reduced blood supply. the cytokines interleukin-1α (il-1α) and il-1β are key contributors to ischemic brain injury. however,there is very little evidence that il-1 expression occurs at the protein level early enough (within hours) to influence brain damage after stroke. in order to determine this we investigated the temporal and spatial profiles of il-1α and il-1β expression after cerebral ischemia.findings: we report here that in mice,as early as 4 h after reperfusion following ischemia induced by occlusion of the middle cerebral artery,il-1α,but not il-1β,is expressed by microglia-like cells in the ischemic hemisphere,which parallels an upregulation of il-1α mrna. 24 h after ischemia il-1α expression is closely associated with areas of focal blood brain barrier breakdown and neuronal death,mostly near the penumbra surrounding the infarct. the sub-cellular distribution of il-1α in injured areas is not uniform suggesting that it is regulated.conclusions: the early expression of il-1α in areas of focal neuronal injury suggests that it is the major form of il-1 contributing to inflammation early after cerebral ischemia. this adds to the growing body of evidence that il-1α is a key mediator of the sterile inflammatory response. © 2011 luheshi et al; licensee biomed central ltd.
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آدرس
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faculty of life sciences,university of manchester, United Kingdom, laboratory of molecular neuroendocrinology,institute of experimental medicine,budapest, Hungary, faculty of life sciences,university of manchester, United Kingdom, faculty of life sciences,university of manchester, United Kingdom, faculty of life sciences,university of manchester,united kingdom,laboratory of molecular neuroendocrinology,institute of experimental medicine,budapest, Hungary
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Authors
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