Stroke is the main cause of morbidity and mortality worldwide. However, the exact molecular mechanism of ischemic stroke has not been fully elucidated. Increasing evidence has indicated that neuroinflammation and neuroimmune plays an important role in pathological injury after ischemic stroke, accompanying with the blood-brain barrier disruption. Immune cells and inflammatory factors—including neutrophils, T cells, B cells, and interleukins, tumor necrosis factor, etc., infiltrate into the postischemic brain tissue, aggravate secondary brain injury in the acute stage of stroke, and promote functional recovery after stroke. However, the relationship and mechanism of these cells and factors have only been partly elucidated.
Clinical trials and animal research support the notion that the immunologic and inflammatory response to acute cerebral ischemia is a major factor in the pathobiology and prognosis of stroke. The immunologic and inflammatory response starts in stenosis or occlusion and hypoperfusion of vessels and ischemic brain parenchyma, and contribute to ischemic damage, but may also be protective. The signaling mechanism underlying brain injury caused by cerebral ischemia is generated in the infarct site propagate through the organism after stroke, leading to a subsequent systemic immunity and inflammatory response, followed by immunosuppression. Animal models are indispensable tools that could mimic these stroke processes and could be used for investigating mechanisms of ischemic cerebral injury and developing novel therapeutic regimens. However, most ischemic strokes occur in the territory of middle cerebral artery (MCA), many animal stroke models that have been developed have focused on this artery. Thus, by using Middle cerebral artery occlusion (MCAO), it is possible to investigate cells and molecules that are important for ischemic damage and use this knowledge to better understand ischemic damage in ischemic stroke with potential therapeutic implications. Some authors have already published relevant results but there are still many gaps in this subject. In addition, the importance of recent findings in the post-stroke immunologic and inflammatory response remains unclear.
For this Research Topic, we welcome submissions of Original Research on the following themes:
• the role of Cytokines and/or molecules play in immunologic and inflammatory response after ischemic stroke
• ischemia-induced inflammation and BBB breakdown involved in ischemic stroke
• strategies targeting neural inflammation after ischemia and reperfusion in order to provide new therapies for stroke
• anti-inflammatory cytokines and neurotrophic factors secreted by activated immune cells that are beneficial for recovery after ischemic stroke
• the double-edged role of the immunologic and inflammatory response in stroke, e.g., when immune cells invade brain, which can contribute to ischemic damage, but may also be protective in the acute phase
• protective effect and mechanism of new neuroprotective drugs on acute ischemic stroke
Stroke is the main cause of morbidity and mortality worldwide. However, the exact molecular mechanism of ischemic stroke has not been fully elucidated. Increasing evidence has indicated that neuroinflammation and neuroimmune plays an important role in pathological injury after ischemic stroke, accompanying with the blood-brain barrier disruption. Immune cells and inflammatory factors—including neutrophils, T cells, B cells, and interleukins, tumor necrosis factor, etc., infiltrate into the postischemic brain tissue, aggravate secondary brain injury in the acute stage of stroke, and promote functional recovery after stroke. However, the relationship and mechanism of these cells and factors have only been partly elucidated.
Clinical trials and animal research support the notion that the immunologic and inflammatory response to acute cerebral ischemia is a major factor in the pathobiology and prognosis of stroke. The immunologic and inflammatory response starts in stenosis or occlusion and hypoperfusion of vessels and ischemic brain parenchyma, and contribute to ischemic damage, but may also be protective. The signaling mechanism underlying brain injury caused by cerebral ischemia is generated in the infarct site propagate through the organism after stroke, leading to a subsequent systemic immunity and inflammatory response, followed by immunosuppression. Animal models are indispensable tools that could mimic these stroke processes and could be used for investigating mechanisms of ischemic cerebral injury and developing novel therapeutic regimens. However, most ischemic strokes occur in the territory of middle cerebral artery (MCA), many animal stroke models that have been developed have focused on this artery. Thus, by using Middle cerebral artery occlusion (MCAO), it is possible to investigate cells and molecules that are important for ischemic damage and use this knowledge to better understand ischemic damage in ischemic stroke with potential therapeutic implications. Some authors have already published relevant results but there are still many gaps in this subject. In addition, the importance of recent findings in the post-stroke immunologic and inflammatory response remains unclear.
For this Research Topic, we welcome submissions of Original Research on the following themes:
• the role of Cytokines and/or molecules play in immunologic and inflammatory response after ischemic stroke
• ischemia-induced inflammation and BBB breakdown involved in ischemic stroke
• strategies targeting neural inflammation after ischemia and reperfusion in order to provide new therapies for stroke
• anti-inflammatory cytokines and neurotrophic factors secreted by activated immune cells that are beneficial for recovery after ischemic stroke
• the double-edged role of the immunologic and inflammatory response in stroke, e.g., when immune cells invade brain, which can contribute to ischemic damage, but may also be protective in the acute phase
• protective effect and mechanism of new neuroprotective drugs on acute ischemic stroke