• Zong-Jian Liu, Chen Chen, Xiao-Rong Li, Yuan-Yuan Ran, Tao Xu, Ying Zhang, Xiao-Kun Geng, Yu Zhang, Hui-Shan Du, Rehana K Leak, Xun-Ming Ji, and Xiao-Ming Hu.
• Institute of Hypoxia Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.
• CNS Neurosci Ther. 2016 Jan 1; 22 (1): 43-52.

AimsRemote ischemic preconditioning (RIPC) of a limb is a clinically feasible strategy to protect against ischemia-reperfusion injury after stroke. However, the mechanism underlying RIPC remains elusive.MethodsWe generated a rat model of noninvasive RIPC by four repeated cycles of brief blood flow constriction (5 min) in the hindlimbs using a tourniquet. Blood was collected 1 h after preconditioning and 3 days after brain reperfusion. The impact of RIPC on immune cell and cytokine profiles prior to and after transient middle cerebral artery occlusion (MCAO) was assessed.ResultsRemote ischemic preconditioning protects against focal ischemia and preserves neurological functions 3 days after stroke. Flow cytometry analysis demonstrated that RIPC ameliorates the post-MCAO reduction of CD3(+)CD8(+) T cells and abolishes the reduction of CD3(+)/CD161a(+) NKT cells in the blood. In addition, RIPC robustly elevates the percentage of B cells in peripheral blood, thereby reversing the reduction in the B-cell population after stroke. RIPC also markedly elevates the percentage of CD43(+)/CD172a(+) noninflammatory resident monocytes, without any impact on the percentage of CD43(-)/CD172a(+) inflammatory monocytes. Finally, RIPC induces IL-6 expression and enhances the elevation of TNF-α after stroke.ConclusionOur results reveal dramatic immune changes during RIPC-afforded neuroprotection against cerebral ischemia.© 2015 John Wiley & Sons Ltd.

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