• J Javier Provencio, Tamer Altay, Saksith Smithason, Shari Korday Moore, and Richard M Ransohoff.
• Neuroinflammation Research Center, Lerner Research Institute, NB3, Cleveland Clinic, 9500 Euclid Ave. Cleveland, OH 44195, United States. provenj@ccf.org
• J. Neuroimmunol. 2011 Mar 1; 232 (1-2): 94-100.

BackgroundThe etiology of delayed cerebral vasospasm (DCV) after aneurysmal subarachnoid hemorrhage (SAH) has remained elusive. Growing evidence supports a role for inflammation in the pathogenesis of DCV. We showed that CSF neutrophils predict which patients will develop DCV.MethodsWe evaluated a murine model of SAH to test the hypothesis that myeloid cells are required for the cerebral damage associated with DCV.ResultsSAH was associated with decreased middle cerebral artery caliber on day 1 which normalized at day 3 and recurred at day 6. In addition, behavioral testing with a Barnes maze showed executive dysfunction that progressively worsened after the seventh day post hemorrhage. To test the role of innate immune responses, we administrated a myeloid cell-depleting monoclonal antibody against Ly6G/C prior to experimental SAH. Myeloid cell depletion ameliorated angiographic vasospasm measured by MCA vessel caliber and normalized behavioral testing.ConclusionOur findings support the role of Ly6G/C(+) cells in the development of DCV after SAH and suggest that immune modulation of neutrophils or other Ly6G/C(+) cells may be a strategy for the prevention of DCV.Copyright © 2010 Elsevier B.V. All rights reserved.

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