Abstract
BackgroundCerebral 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.FindingsWe 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.ConclusionsThe 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.
Highlights
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 early expression of IL-1a in areas of focal neuronal injury suggests that it is the major form of IL1 contributing to inflammation early after cerebral ischemia
This adds to the growing body of evidence that IL-1a is a key mediator of the sterile inflammatory response
Summary
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. Conclusions: The early expression of IL-1a in areas of focal neuronal injury suggests that it is the major form of IL1 contributing to inflammation early after cerebral ischemia. Ac.uk † Contributed 1Faculty of Life Sciences, University of Manchester, UK Full list of author information is available at the end of the article reduced when administration is delayed beyond 3 h [4], suggesting that IL-1 expressed early after the insult is important.
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