Reparative System Arising from CCR2(+) Monocyte Conversion Attenuates Neuroinflammation Following Ischemic Stroke

Joohyun Park, Jong Youl Kim, Yu Rim Kim, Meiying Huang, Ji Young Chang, A Young Sim, Hosung Jung, Won Taek Lee, Young-Min Hyun, Jong Eun Lee
2021 Translational Stroke Research  
AbstractMonocytes recruitment from the blood to inflamed tissues following ischemic stroke is an important immune response to wound healing and tissue repair. Mouse monocytes can be endogenously divided into two distinct populations: pro-inflammatory or classical monocytes that express CCR2highCX3CR1low and circulate in blood, and anti-inflammatory or non-classical monocytes that express CCR2lowCX3CR1high and patrol locally. In this study of transgenic mice with functional CX3CR1GFP/+ or
more » ... 3CR1GFP/+ or CX3CR1GFP/+-CCR2RFP/+, we found that CCR2highCX3CR1low monocytes recruited to the injured brain were cytokine-dependently converted into CCR2lowCX3CR1high macrophages, especially under the influence of IL-4 and IL-13, thereby attenuating the neuroinflammation following sterile ischemic stroke. The overall data suggest that (1) the regulation of monocyte-switching is one of the ultimate reparative strategies in ischemic stroke, and (2) the adaptation of monocytes in a locally inflamed milieu is vital to alleviating the effects of ischemic stroke through innate immunity.
doi:10.1007/s12975-020-00878-x pmid:33409730 fatcat:n7xwl5wxrbakfm2ferurr7qpfy