Dear Colleagues,

Ischemic stroke is caused by a reduction in blood flow to the brain, and it is a major cause of mortality and disability worldwide.

The most upstream consequence of cerebral ischemia, fundamentally, is composed of an energetic problem. Once this initial step has taken place, an ischemic cascade follows, involving a multimodal and multicell series of downstream mechanisms.

Inflammation is an important part of stroke pathophysiology, especially in the context of reperfusion. Several studies have shown that a nonspecific systemic inflammatory response occurs after both ischemic and hemorrhagic stroke, proving that inflammatory mechanisms intrinsic to the brain and the blood are among the important mediators of focal cerebral injury. The immune system is actively involved in the pathogenesis of acute brain damage through some events, such as leukocyte and monocyte infiltration into the brain; the activation of resident cells, including microglia, astrocytes, and endothelial cells; and several high serum levels.

Animal models of focal ischemia induced by middle cerebral artery occlusion (MCAO) provide evidence for most of the cellular inflammatory responses in stroke.

We will review the role of inflammatory cytokines in the pathogenesis of ischemic neuronal damage. We will also review the involvement of microglial, which are the major resident immune cells in CNS, and play a critical role in the immune response to a variety of events including infection, trauma, stroke, and neurogeneration. Among the various types of circulating leukocytes, neutrophils are generally the first leukocyte subtype recruited to the ischemic brain, and we will review their role in ischemic stroke pathogenesis. The inflammatory responses of the brain to post ischemia are characterized by the involvement of different subtypes of T lymphocytes, which contribute to the pathogenesis of stroke-induced microvascular dysfunction and tissue damage. We also will review the role of T lymphocytes and of their subsets. T cells can be separated into three major groups based on function, as follows: cytotoxic T cells (CD8+), helper T cells (Th; CD4+), and regulatory T cells (Tregs). We will review the literature on the available data concerning their involvement in ischemic stroke pathogenesis. We will also review the role of inflammatory mediators in a particular subtype of ischemic stroke, such as cardioembolic and atherosclerotic ones.

Prof. Dr. Antonino Tuttolomondo
Guest Editor

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