The effects of bone marrow derived macrophages on ischemic brain damage

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Cerebral ischemia triggers acute inflammation, which exacerbates primary brain damage. Activation of the innate immune system is an important component of this inflammatory response. Inflammation occurs through the action of proinflammatory cytokines. Production of these cytokines is initiated by signaling through Toll-like receptors (TLRs). Among them, TLR4 recognizes primarily lipopolysaccharide (LPS) and an increasing evidence points that TLR4 plays a crucial role in the concert mechanism of the cerebra ischemia. In this study, we investigated the effect of targeted disruption of TLR4 on the severity of ischemic brain injury. TLR4 ablation significantly decreased infarct size at 1 day after reperfusion. The amelioration of tissue damage in the absence of TLR4 underscores the importance of innate immunity for the manifestation of ischemic brain injury. Furthermore, TLR4 ablation in the bone marrow derived macrophage significantly decreased infarct size. These results indicate that bone barrow derived macrophages are an important modulator of ischemic brain injury.