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Review
. 2022 May;53(5):1460-1472.
doi: 10.1161/STROKEAHA.121.036948. Epub 2022 Apr 5.

Neuroinflammation, Stem Cells, and Stroke

Stefan Anthony #  1 , Dorothy Cabantan #  1 , Molly Monsour #  2 , Cesario V Borlongan  2
Affiliations
Review

Neuroinflammation, Stem Cells, and Stroke

Stefan Anthony et al. Stroke. 2022 May.

Abstract

Stroke remains a significant unmet clinical need with few treatment options that have a very narrow therapeutic window, thereby causing massive mortality and morbidity in the United States and around the world. Accordingly, finding safe and effective novel treatments with a wider therapeutic window stands as an urgent need in stroke. The progressive inflammation that occurs centrally and peripherally after stroke serves as a unique therapeutic target to retard and even halt the secondary cell death. Stem cell therapy represents a potent approach that can diminish inflammation in both the stroke brain and periphery (eg, spleen), advancing a paradigm shift from a traditionally brain-focused therapy to treating stroke as a neurological disorder with a significant peripheral pathology. The purpose of this review article is to highlight the inflammation-mediated secondary cell death that plagues both brain and spleen in stroke and to evaluate the therapeutic potential of stem cell therapy in dampening these inflammatory responses.

Keywords: blood-brain barrier; central nervous system; hemorrhage; inflammation; interleukin.

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Figures

Figure 1.
Figure 1.. Timeline of stroke-induced inflammation.
The stages of inflammation in stroke can be delineated as acute, subacute, and chronic.
Figure 2.
Figure 2.. Stem cell grafts alleviate stroke chronic inflammation in brain and spleen.
Stroke renders inflammatory responses from the brain and the spleen, creating a brain-spleen coupling of central and peripheral inflammation that exacerbates the secondary cell death. Intravenously transplanted stem cells migrate preferentially to the spleen with a few cells reaching the brain, altogether conferring direct and indirect sequestration of the inflammation-plagued secondary cell death in stroke.
See this image and copyright information in PMC

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