Abstract
Intravenous immunoglobulin (IVIG) may improve neuroinflammation after traumatic brain injury (TBI). IVIG administration after TBI improved rotarod latencies over the first 7days (p=0.039) and water maze latencies over 29–32days (p=0.027), decreased F4/80-positive cells at 2 (p=0.001) and 7days (p<0.001), decreased Fluoro-Jade B-positive cells (p=0.020), increased NeuN-positive cells (p=0.014), decreased IL-6 production at 4 (p=0.032) and 24h (p=0.023), and decreased blood–brain barrier breakdown by IgG extravasation (p=0.001) and brain edema (p=0.006); however, TNF-α concentration was unchanged. IVIG administration was associated with long-term neurobehavioral and histological improvement through modulation of neuroinflammation and blood–brain barrier permeability in a murine TBI model.
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