We are analyzing https://link.springer.com/article/10.1007/s10571-020-00966-4.

Title:
Role of DAMPs and of Leukocytes Infiltration in Ischemic Stroke: Insights from Animal Models and Translation to the Human Disease | Cellular and Molecular Neurobiology
Description:
Stroke is a leading cause of death and disability worldwide. Several mechanisms are involved in the pathogenesis of ischemic stroke (IS). The contributory role of the inflammatory and immunity processes was demonstrated both in vitro and in animal models, and was confirmed in humans. IS evokes an immediate inflammatory response that involves complex cellular and molecular mechanisms. All components of the innate and adaptive immunity systems are involved in several steps of the ischemic cascade. In the early phase, inflammatory and immune mechanisms contribute to the brain tissue damage, whereas, in the late phase, they participate to the tissue repair processes. In particular, damage-associated molecular patterns (DAMPs) appear critical for the promotion of altered blood brain barrier permeability, leukocytes infiltration, tissue edema and brain injury. Conversely, the activation of regulatory T lymphocytes (Tregs) plays protective effects. The identification of specific cellular/molecular elements belonging to the inflammatory and immune responses, contributing to the brain ischemic injury and tissue remodeling, offers the advantage to design adequate therapeutic strategies. In this article, we will present an overview of the knowledge on inflammatory and immunity processes in IS, with a particular focus on the role of DAMPs and leukocytes infiltration. We will discuss evidence obtained in preclinical models of IS and in humans. The main molecular mechanisms useful for the development of novel therapeutic approaches will be highlighted. The translation of experimental findings to the human disease is still a difficult step to pursue. Further investigations are required to fill up the existing gaps.
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Keywords {🔍}

pubmed, article, google, scholar, cas, stroke, central, ischemic, brain, cerebral, ischemia, acute, role, cell, inflammation, immune, injury, med, blood, httpsdoiorg, httpsdoiorgs, inflammatory, cells, neurol, molecular, rat, chen, zhang, liu, yang, zhou, damps, immunity, therapeutic, receptor, nat, shock, transient, neurosci, group, box, hmgb, human, disease, damage, regulatory, focal, signaling, protein, models,

Topics {✒️}

month download article/chapter blood–brain barrier breakdown c-reactive protein concentration connolly es jr ifn-gamma mrna expression cytokine-induced endothelial cells writing—original draft preparation p-selectin deficient mice acute anti-inflammatory approaches phthalide derivative cd21 intercellular adhesion molecule-1 adaptive dose-response study individual participant meta-analysis trif-adaptor independent toll full article pdf reperfusion injury induced chronic cerebrovascular disease acute cerebral infarction toledo-pereyra lh photochemically induced ischemia heat shock proteins signaling pathway blockade microvascular dysfunction induced privacy choices/manage cookies anti-vcam-1 antibodies anti-icam-1 therapy todd rf 3rd anti-leukocyte antibodies brain ischemic injury ischemic brain injury post-ischemic inflammation uric acid promotes tissue repair processes article cellular focal cerebral ischemia immunomodulatory therapeutic strategies neuronal cell death global cerebral ischemia article stanzione american heart association conditions privacy policy steady plasma concentration brain tissue damage central role lymphocyte trafficking shields local immune responses li yj transient ischemic stroke involves complex cellular early release

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         Neurobiology
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