| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3063978 | Journal of Neuroimmunology | 2014 | 7 Pages |
•Efficacy of IVIG administration was assessed after traumatic brain injury in mice.•After TBI in mice, IVIG decreased blood–brain barrier permeability.•After TBI in mice, IVIG decreased microglial activation/macrophage recruitment.•After TBI in mice, IVIG improved long-term neurobehavioral outcome.•With defined dosing parameters, IVIG may translate into an acute treatment for TBI.
Intravenous immunoglobulin (IVIG) may improve neuroinflammation after traumatic brain injury (TBI). IVIG administration after TBI improved rotarod latencies over the first 7 days (p = 0.039) and water maze latencies over 29–32 days (p = 0.027), decreased F4/80-positive cells at 2 (p = 0.001) and 7 days (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 24 h (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.
