Neuroinflammation and brain–peripheral interaction in ischemic stroke: A narrative review

Abstract

Excessive immune activation within the lesion site can be observed after stroke onset. Such neuroinflammation within the brain parenchyma represents the innate immune response, as well as the result of the additional interactions between peripheral and resident immune cells. Accumulative studies have illustrated that the pathological process of ischemic stroke is associated with resident and peripheral immunity. The infiltration of peripheral immune cells within the brain parenchyma implicitly contributes to secondary brain injuries. Therefore, better understanding of the roles of resident and peripheral immune reactions toward ischemic insult is necessary. In this review, we summarized the interaction between peripheral and resident immunity on systemic immunity and the clinical outcomes after stroke onset and also discussed various potential immunotherapeutic strategies.

Selected serum cytokines and vitamin D levels as potential prognostic markers of acute ischemic stroke

“…In Acute Ischemic Stroke (AIS), this Inflammation leads to oxidative stress, which is postulated to contribute to neuronal damage, leading to poor clinical outcomes [ 1 ]. AIS-associated neuroinflammation is mediated by activated brain-residing astrocytes, microglial cells, and infiltrating T lymphocytes [ 2 ]. In AIS, abnormalities in peripheral immune functions, such as changes in lymphocyte subpopulations in blood, deviation of T-lymphocyte subsets, damage to the blood-brain barrier (BBB), and increased cytokine levels have been reported [ 3 ].…”