Abstract TP270: Ischemic Preconditioning-afforded Neuroprotection Against Ischemic Stroke is Associated With Altered Peripheral Immune Responses

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The limb remote ischemic preconditioning (RIPC) is considered a clinical feasible protective strategy against ischemia-reperfusion injury after stroke. However, its mechanisms of protection remain elusive. Here, we used a rat model of non-invasive RIPC by tourniquet to study the impact of RIPC on the immune cell and cytokine profiles after transient middle cerebral artery occlusion. Our data indicates that RIPC protects against focal ischemia and preserves neurological functions 3 days after stroke. Meanwhile, RIPC results in dramatic changes in several immune cell populations after stroke. Specifically, the RIPC ameliorated the post-MCAO reduction of blood CD3+CD8+ T cells and abolished the reduction of CD3+/CD161a+ NKT cells. Another striking change is that RIPC significantly elevated the B cell percentage in peripheral blood, which reversed the otherwise reduced B cell population after stroke. RIPC also markedly elevated the percentage of CD43+/CD172a+ non-inflammatory residential monocytes, while showing no effect on the percentage CD43-/CD172a+ inflammatory monocytes. In addition, we found that RIPC induced IL-6 expression and enhanced the elevation of TNFα after stroke. Collectively, our results reveal potential immune mechanisms of RIPC-afforded neuroprotection against cerebral ischemia. Further exploration about these immune elements in RIPC-afforded ischemic tolerance may lead to the development of systemically administered immune therapies for stroke patients.

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