Cellular inflammatory response associated with breakdown of the blood-brain barrier after closed head injury in rats
Abstract
This study reports a widespread microglial response characterized by an upregulation of surface antigens, such as complement type 3 receptors (CR3) and major histocompatibility complex (MHC) class II antigens on these cells following closed head injury. Increased expression of CR3 (OX-42) and MHC class II antigens (OX-6) was observed in rats killed at 1, 3, and 5 days after injury. Intense OX-42 immunoreactivity was observed in microglial cells throughout the brain with a smaller number of them being OX-6 positive. In addition to microglial reaction, astrocytic activation reflected in cellular hypertrophy and increased immunoreactivity for glial fibrillary acidic protein (GFAP) was observed at 5 days after head injury. Together with the above, a diffuse perivascular and intraneuronal immunostaining for immunoglobulin G (IgG) was observed primarily in the cerebral cortex. This was accompanied by an enhanced expression of both endothelial nitric oxide synthase (eNOS) in blood vessels and inducible nitric oxide synthase (iNOS) in brain macrophages. In rats subjected to closed head injury followed by a single intraperitoneal (i.p.) injection of rhodamine isothiocyanate (RhIc), seepage of the fluorescent dye into the neuropil was ob...Continue Reading
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