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Review
. 2019 May 28:13:540.
doi: 10.3389/fnins.2019.00540. eCollection 2019.

The Inflammatory Response After Ischemic Stroke: Targeting β2 and β1 Integrins

Danielle N Edwards  1   2 , Gregory J Bix  3   4
Affiliations
Review

The Inflammatory Response After Ischemic Stroke: Targeting β2 and β1 Integrins

Danielle N Edwards et al. Front Neurosci. .

Abstract

Ischemic stroke is a leading cause of death and disability with limited therapeutic options. Resulting inflammatory mechanisms after reperfusion (removal of the thrombus) result in cytokine activation, calcium influx, and leukocytic infiltration to the area of ischemia. In particular, leukocytes migrate toward areas of inflammation by use of integrins, particularly integrins β1 and β2. Integrins have been shown to be necessary for leukocyte adhesion and migration, and thus are of immediate interest in many inflammatory diseases, including ischemic stroke. In this review, we identify the main integrins involved in leukocytic migration following stroke (α L β2, αDβ2, α4β1, and α5β1) and targeted clinical therapeutic interventions.

Keywords: clinical trial results; inflammation; integrins; ischemic stroke; leukocytes.

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Figures

FIGURE 1
FIGURE 1
Representative diagram of regions of interest on activated leukocytes.
FIGURE 2
FIGURE 2
Representative image of the β2 integrin response following experimental stroke and inhibitory antibody treatment in preclinical trials. Inhibition of (A) αLβ2 and (B) αMβ2 integrins post-stroke responses and effects.
FIGURE 3
FIGURE 3
Representative image of the β1 integrin response following experimental stroke and inhibitory antibody treatment in preclinical trials. Inhibition of (A) α4β1 and (B) α5β1 integrins post-stroke responses and effects.
See this image and copyright information in PMC

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References

    1. Arnaout M. A. (1990). Leukocyte adhesion molecules deficiency: its structural basis, pathophysiology and implications for modulating the inflammatory response. Immunol. Rev. 114 145–180. 10.1111/j.1600-065x.1990.tb00564.x - DOI - PubMed
    1. Arumugam T. V., Salter J. W., Chidlow J. H., Ballantyne C. M., Kevil C. G., Granger D. N. (2004). Contributions of LFA-1 and Mac-1 to brain injury and microvascular dysfunction induced by transient middle cerebral artery occlusion. Am. J. Physiol. Heart Circ. Physiol. 287 H2555–H2560. 10.1152/ajpheart.00588.2004 - DOI - PubMed
    1. Aspey B., Jessimer C., Pereira S., Harrison M. (1989). Do leukocytes have a role in the cerebral no-reflow phenomenon? J. Neurol. Neurosurg. Psychiatry 52 526–528. 10.1136/jnnp.52.4.526 - DOI - PMC - PubMed
    1. Bargatze R., Kurk S., Butcher E., Jutila M. (1994). Neutrophils roll on adherent neutrophils bound to cytokine-induced endothelial cells via L-selectin on the rolling cells. J. Exp. Med. 180 1785–1792. 10.1084/jem.180.5.1785 - DOI - PMC - PubMed
    1. Becker K. (2002). Anti-leukocyte antibodies: leukarrest (Hu23F2G) and enlimomab (R6.5) in acute stroke. Curr. Med. Res. Opin. 18(Suppl. 2), 18–22. - PubMed

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