Authors: Saksith Smithason Shari Korday Moore J Javier Provencio
Publish Date: 2011/11/17
Volume: 16, Issue: 2, Pages: 327-334
Abstract
Delayed deterioration associated with vasospasm DDAV after aneurismal subarachnoid hemorrhage SAH is a major cause of morbidity We have previously shown that myeloid cell depletion before experimental SAH in a murine model ameliorates DDAV In this study we address whether systemic administration of lipopolysaccharide LPS worsens DDAV in a myeloid celldependent fashionWe challenged mice in our experimental SAH model with LPS before hemorrhage and evaluated the degree of vasospasm on day 6 with India ink angiography behavioral deficits by rotorod Ymaze and Barnes maze testing microglial activation early after SAH by immunohistochemistry and the brain levels of the chemokines CCL5 and KC at the time of vasospasm Another group of animals were given the myeloid celldepleting antibody against the neutrophil antigen Ly6G/C prior to LPS administration and SAHLPS followed by SAH significantly worsens angiographic vasospasm as well as performance on the Barnes maze but not the Ymaze or rotorod tests There was an increased activation of microglia in animals with LPS before SAH compared to SAH alone Depletion of myeloid cells before LPS administration inhibited the development of vasospasm improved the performance on behavioral tests and reduced microglial activation The chemokines CCL5 and KC were incrementally elevated in SAH and LPS SAH but suppressed in animals with myeloid cell depletion
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