The Contribution of Mannose Binding Lectin to Reperfusion Injury after Ischemic Stroke

Author(s): Helena Morrison, Jennifer Frye, Grace Davis-Gorman, Janet Funk, Paul McDonagh, Gregory Stahl, Leslie Ritter

Journal Name: Current Neurovascular Research

Volume 8 , Issue 1 , 2011

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After complement system (CS) activation, the sequential production of complement products increases cell injury and death through opsonophagocytosis, cytolysis, adaptive, and inflammatory cell responses. These responses potentiate cerebral ischemia-reperfusion (IR) injury after ischemic stroke and reperfusion. Activation of the CS via mannose binding lectin (MBL)-initiated lectin pathway is known to increase tissue damage in response to IR in muscle, myocardium and intestine tissue. In contrast, the contribution of this pathway to cerebral IR injury, a neutrophil-mediated event, is less clear. Therefore, we investigated the potential protective role of MBL deficiency in neutrophil-mediated cerebral injury after IR. Using an intraluminal filament method, neutrophil activation and cerebral injury were compared between MBL-deficient and wild type C57Bl/6 mice subjected to 60 minutes of MCA ischemia and reperfusion. Systemic neutrophil activation was not decreased in MBL-deficient animals after IR. In MBL-deficient animals, cerebral injury was significantly decreased only in the striatum (p < 0.05). Despite MBL deficiency, C3 depositions were evident in the injured hemisphere during reperfusion. These results indicate that while MBL deficiency results in a modest protection of a sub-cortical brain region during IR, redundant complement pathway activation may overwhelm further beneficial effects of MBL deficiency during reperfusion.

Keywords: Complement, ischemia, mannose binding lectin, neutrophil, reperfusion, stroke

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Article Details

Year: 2011
Page: [52 - 63]
Pages: 12
DOI: 10.2174/156720211794520260

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