Immunity in Stroke: The Next Frontier

Abstract

Translational stroke research has long been focusing on neuroprotective strategies to prevent secondary tissue injury and promote recovery after acute ischemic brain injury. The inflammatory response to stroke has more recently emerged as a key pathophysiological pathway contributing to stroke outcome. It is now accepted that the inflammatory response is functionally involved in all phases of the ischemic stroke pathophysiology. The immune response is therefore considered a breakthrough target for ischemic stroke treatment. On one side, stroke induces a local neuroinflammatory response, in which the inflammatory activation of glial, endothelial and brain-invading cells contributes to lesion progression after stroke. On the other side, ischemic brain injury perturbs systemic immune homeostasis and results in long-lasting changes of systemic immunity. Here, we briefly summarize current concepts in local neuroinflammation and the systemic immune responses after stroke, and highlight two promising therapeutic strategies for poststroke inflammation.

Depletion of Arg1-Positive Microglia/Macrophages Exacerbates Cerebral Ischemic Damage by Facilitating the Inflammatory Response

“…Arg1 expression is upregulated in some cells when individuals undergo tissue injury, such as injury-induced activated inflammatory cells. It is well known that cerebral ischemia leads to intense and persistent inflammation, affecting the progression of pathology [ 1 , 39 ]. Although detailed experimental and clinical information on the role of Arg in ischemic stroke is limited, data suggest an increase in Arg activity after cerebral ischemia [ 40 ].…”

“…Ischemic stroke is a common cerebrovascular disease with a high mortality and disability rate. In addition to causing neuronal damage, it is recognized that cerebral ischemia triggers systemic and intracerebral inflammatory responses [ 1 , 2 , 3 ]. The increase and activation of inflammatory cells and the production and release of inflammatory cytokines are important factors influencing the progression of the disease.…”

Association of bioimpedance analysis parameters trajectories with clinical outcomes in neurocritical patients

“…The prognosis of neurocritical patients is influenced by pre-existing physical health status, the severity of primary brain injury and the trend of secondary brain injury development. In particular, the dynamic changes in inflammatory response and nutritional status in the acute phase (1–7 days after onset) play a key role in the mechanism of secondary brain injury and disease progression [ [7] , [8] , [9] , [10] ]. The identification of acute phase nutritional and inflammatory status within 1–7 days after admission for neurocritical patients and the observation of trends in their changes may have positive implications for adjusting their treatment plans and improving clinical outcomes.…”

Plasma S100A1 protein: An effective prognostic biomarker for 3-month clinical outcome in acute ischemic stroke patients

“…The immune-inflammatory response is one of the pathophysiological foundations of AIS and plays a role in each stage of the AIS pathogenesis. 9 As a result, the immuneinflammatory response is also recognized as an important target for diagnosing and treating acute ischemic stroke. Firstly, stroke induces a localized neuroinflammatory response, where the inflammatory activation of glial, endothelial, and brain-invading cells contributes to the progression of the post-stroke lesion.…”

“…Secondly, ischemic brain injury disrupts the homeostasis of the systemic immune system, resulting in enduring modifications. 9 When an ischemic stroke occurs, a massive variety of biochemical and inflammatory mediators, including cytokines, chemokines, and pro-inflammatory enzymes, are produced. 10,11 S100A1 protein is a recently identified novel inflammatory marker and a member of the S100 protein family.…”