J Cerebrovasc Endovasc Neurosurg > Epub ahead of print
DOI: https://doi.org/10.7461/jcen.2021.E2021.04.003    [Epub ahead of print]
Published online September 23, 2021.
Systemic macrophage depletion attenuates infarct size in an experimental mouse model of stroke
Seung-Won Lee1, Dong-Jun Song2, Han-Seung Ryu1, You-Sub Kim1, Tae-Sun Kim1, Sung-Pil Joo1 
1Department of Neurosurgery, Chonnam National University Hospital and Medical School, Gwangju, Korea
2Department of Biomedical Sciences, Chonnam National University, Gwangju, Korea
Correspondence:  Sung-Pil Joo, Tel: +82-62-220-6608, Fax: +82-62-224-9865, 
Email: nsjsp@hanmail.net
Received: 26 April 2021   • Revised: 8 July 2021   • Accepted: 14 July 2021
Abstract
Objective
Macrophages have been shown to play important roles in various pathophysiological processes of the central nervous system via neuroinflammation, leading to an increased interest in macrophage biology. Circulating blood monocytes are among the first cells to infiltrate the brain after ischemic stroke; however, the role of innate immune cells such as monocytes and macrophages remains to be elucidated. Here, we investigated the association between blood monocytes and infarct size following ischemic stroke.
Methods
We induced stroke using a focal ischemia mouse model through middle cerebral artery suture occlusion. To deplete circulating blood monocytes, clodronate was injected intraperitoneally 24 h before the surgery. Animals were sacrificed at specified time points, and the infarct size and mRNA expression were then measured.
Results
The clodronate-injected mice showed significantly smaller infarct size than the control mice. Immunohistochemical staining revealed that monocyte depletion significantly blocked the infiltration of macrophages and microglia. The mRNA expression levels of macrophage and microglia markers were higher in the left infarcted brain than in the right non-infarcted brain.
Conclusions
In summary, monocyte depletion reduced the infarct size and mitigated neurological deficits in mice following ischemic stroke, likely by blocking the infiltration of inflammatory cells such as macrophages and microglia.
Key Words: Cerebral ischemia, Clodronate, Macrophages, Microglia, Infarction
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ORCID iDs

Sung-Pil Joo
https://orcid.org/0000-0002-4983-0174

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