Abstract
One of the leading causes of neurological mortality, disability, and dementia worldwide is cerebral ischemia. Among the many pathological phenomena, the immune system plays an important role in the development of post-ischemic degeneration of the brain, leading to the development of neuroinflammatory changes in the brain. After cerebral ischemia, the developing neuroinflammation causes additional damage to the brain cells, but on the other hand it also plays a beneficial role in repair activities. Inflammatory mediators are sources of signals that stimulate cells in the brain and promote penetration, e.g., T lymphocytes, monocytes, platelets, macrophages, leukocytes, and neutrophils from systemic circulation to the brain ischemic area, and this phenomenon contributes to further irreversible ischemic brain damage. In this review, we focus on the issues related to the neuroinflammation that occurs in the brain tissue after ischemia, with particular emphasis on ischemic stroke and its potential treatment strategies.
Highlights
Laboratory of Ischemic and Neurodegenerative Brain Research, Mossakowski Medical Research Institute, Department of Pathophysiology, Medical University of Lublin, PL 20-090 Lublin, Poland; Abstract: One of the leading causes of neurological mortality, disability, and dementia worldwide is cerebral ischemia
The risk of ischemic stroke is age-related, with about 75% of all cases occurring in patients over 64 years of age, and about 25% of cases occurring in young people, suggesting that the pathology does affect the elderly [8]
The exact relationship between pro- and antiinflammatory cytokines and their relevance to clinical outcomes in ischemic stroke patients remain unexplained. This balance is disturbed in the early stages of an ischemic stroke [8]. This supports the study of elevated pro-inflammatory IL-6 in the blood at 12 h after cerebral ischemia in stroke patients compared to controls, and this increase has been correlated with severe neurological deficits and worse outcomes [50]
Summary
Numerous studies have shown an inflammatory response in brain tissue to local or complete ischemia in animals and humans [8,26,27,41,42,43,44,45]. Inflammation following ischemic brain injury in rats surviving 2 years after global cerebral ischemia showed different severity of microglia and astrocyte responses in different brain structures In these animals, the study revealed significant astrocyte activation in the CA1 and CA3 areas of the hippocampus and the dentate gyrus, in the motor and sensory cortex, and in the striatum and thalamus, while microglial activation was only seen in the CA1 and CA3 areas of the hippocampus and in the motor cortex. The above observations indicate a persistent dysfunction of the blood–brain barrier, which in the long run may still allow T lymphocytes to pass from the blood to the post-ischemic brain Such processes are supported by microglia activity up to 2 years after ischemia [27]. These cytokines are involved in the progression of post-ischemic brain neurodegeneration and influence disease severity and neurological outcomes [8,41]
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