RESUMO
Postinjury inflammation has been implicated in secondary degeneration following injury to the spinal cord. The cellular inflammatory response to injury has not been described in the lateral compression injury model, although various types of compression injuries account for â¼20% of human spinal cord injuries (SCI). Here, we used forceps to induce a moderate compression injury to the thoracic spinal cord of female Sprague-Dawley rats. We evaluated innate and adaptive components of the inflammatory response at various times postinjury using immunohistochemical techniques. We show that components of innate immunity (e.g., macrophages and dendritic cells) peak between 1 and 2 weeks postinjury but persist through 42 days postinjury (dpi). CD163 and CD206 expression, associated with an anti-inflammatory, reparative phenotype, was upregulated on activated macrophages in the injury site, as were MHC class II antigens. The expression of MHC class II antigens is necessary for the initiation of adaptive immunity and was accompanied by an influx of T cells. T cells were initially restricted to gray matter at the injury epicenter but were later observed throughout the lesioned parenchyma. In summary, we demonstrate that lateral forceps compression of the spinal cord produces a neuroinflammatory response similar to that described in human spinal cord trauma and in other experimental models of spinal cord trauma, thus is an appropriate model to study secondary neurodegeneration in SCI.
Assuntos
Mielite/etiologia , Mielite/patologia , Compressão da Medula Espinal/complicações , Compressão da Medula Espinal/patologia , Traumatismos da Medula Espinal/complicações , Traumatismos da Medula Espinal/patologia , Animais , Antígenos CD/metabolismo , Antígenos de Diferenciação Mielomonocítica/metabolismo , Modelos Animais de Doenças , Feminino , Antígenos de Histocompatibilidade Classe II/metabolismo , Imunidade Inata , Lectinas Tipo C/metabolismo , Macrófagos/metabolismo , Macrófagos/patologia , Receptor de Manose , Lectinas de Ligação a Manose/metabolismo , Mielite/metabolismo , Ratos , Ratos Sprague-Dawley , Receptores de Superfície Celular/metabolismo , Compressão da Medula Espinal/metabolismo , Traumatismos da Medula Espinal/metabolismo , Instrumentos Cirúrgicos/efeitos adversos , Linfócitos T/metabolismo , Linfócitos T/patologia , Vértebras TorácicasRESUMO
Controversy exists over the role of autoantibodies to central nervous system antigens in autism and Tourette Syndrome. We investigated plasma autoantibody titers to glial fibrillary acidic protein (GFAP) in children with classic onset (33) and regressive onset (26) autism, controls (25, healthy age- and gender-matched) and individuals with Tourette Syndrome (24) by enzyme-linked immunosorbent assays. We found a significant difference in autoantibody titers to GFAP, not accounted for by age, between the Tourette (significantly lower) and regressive autism groups. However, no differences were found between: classic/regressive; classic/controls; classic/Tourette; regressive/controls; or controls/Tourette. Autoantibody responses against GFAP are unlikely to play a pathogenic role in autism or Tourette Syndrome.
Assuntos
Transtorno Autístico/imunologia , Autoanticorpos/sangue , Proteína Glial Fibrilar Ácida/imunologia , Síndrome de Tourette/imunologia , Transtorno Autístico/diagnóstico , Encéfalo/imunologia , Criança , Pré-Escolar , Ensaio de Imunoadsorção Enzimática , Feminino , Humanos , Masculino , Valores de Referência , Síndrome de Tourette/diagnósticoRESUMO
Autoantibodies to central nervous system antigens, such as myelin basic protein (MBP), may play a role in autism. We measured autoantibody titers to MBP in children with autism, both classic onset and regressive onset forms, controls (healthy age- and gender-matched) and individuals with Tourette syndrome via enzyme-linked immunosorbent assays. We found a significant difference in autoantibody titers to MBP, not accounted for by age or medication, between Tourette and classic autism (both significantly lower) when compared to regressive autism, but not when compared to controls. Autoantibody responses against MBP are unlikely to play a pathogenic role in autism.