Autor: |
Luheshi Nadia M, Kovács Krisztina J, Lopez-Castejon Gloria, Brough David, Denes Adam |
Jazyk: |
angličtina |
Rok vydání: |
2011 |
Předmět: |
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Zdroj: |
Journal of Neuroinflammation, Vol 8, Iss 1, p 186 (2011) |
Druh dokumentu: |
article |
ISSN: |
1742-2094 |
DOI: |
10.1186/1742-2094-8-186 |
Popis: |
Abstract 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. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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