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CD36: An Inflammatory Mediator in Acute Brain Injury

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Immunological Mechanisms and Therapies in Brain Injuries and Stroke

Part of the book series: Springer Series in Translational Stroke Research ((SSTSR,volume 6))

Abstract

Stroke is a major leading cause of death and disability in the human population. The pathology of stroke-induced brain injury involves multifactorial pro-death processes. Among them, inflammation is an important contributor to stroke pathology as indicated by the close association between excessive inflammation and exacerbation of the disease process. Considerable experimental evidence indicates that disease outcome is modulated by several factors including predisposing clinical conditions. Stroke compromises vascular permeability and leads to breakdown of the blood–brain barrier. While the pathology primarily occurs in the CNS, the presence of peripheral immune cells in the infarcted area suggests their potential role in post-ischemic inflammation. Given recent advances highlighting the heterogeneity of peripheral immune cells and diversity of their function, we review neuroimmune interaction in the setting of acute cerebral ischemia, post-ischemic inflammation, and the trafficking of peripheral immune cells to inflamed tissue, with specific focus on the involvement of the class B scavenger receptor, CD36. We discuss CD36 expression and functions, the contribution of the receptor to stroke pathology, its relevance to peripheral inflammatory conditions, and potential strategies to target the CD36-associated neuroinflammatory pathway.

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Abbreviations

AGE:

Advanced glycation end product

BBB:

Blood–brain barrier

CCR2:

c–c chemokine receptor type 2

DAMP:

Damage-associated molecular pattern

EAE:

Experimental autoimmune encephalitis

fΑβ:

Fibrillar beta-amyloid

ICAM:

Intercellular adhesion molecule

MCP-1:

Monocyte chemotactic protein-1

mLDL:

Modified low-density lipoprotein

oxLDL:

Oxidized low-density lipoprotein

ox PC CD36 :

Oxidized choline glycerophospholipid species

PAMP:

Pathogen-associated molecular pattern

PPAR-Îł:

Peroxisome proliferator-activated receptor-Îł

PRR:

Pattern recognition receptor

TLR:

Toll-like receptors

TSPs:

Thrombospondins

SAB:

Salvianolic acid B

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Cho, S., Febbraio, M. (2014). CD36: An Inflammatory Mediator in Acute Brain Injury. In: Chen, J., Hu, X., Stenzel-Poore, M., Zhang, J. (eds) Immunological Mechanisms and Therapies in Brain Injuries and Stroke. Springer Series in Translational Stroke Research, vol 6. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-8915-3_18

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