3.2.5. Macrophages

Circulating macrophages are involved in delayed development of the neuroinflammatory mechanism in an ischemic brain. As early as 2 h after ischemia, activated macrophages can be detected in the brain [100]. Between 22 and 46 h after ischemia, both blood-born and brain-resident macrophages are dispersed throughout the ischemic injury in the brain and remain detectable for up to 1 week in mice after a 30 min ischemic injury [100]. In another study, their presence in brain tissue was recorded 4 days after the onset of ischemia, peaking after 7 days and then diminishing [55]. Pathological post-stroke mechanisms aggravate cell damage due to primary cellular events that initiate a vicious pathological cycle of inflammatory mediators that further enhances neuronal death. In summary, all the inflammatory cells described above play an important role both in initiating and enhancing the pathological response following brain ischemia, but also in maintaining homeostasis of brain cells, especially neurons that have survived a primary ischemic event.
