title: Acute inflammatory responses to mechanical lesions in the CNS: differences between brain and spinal cord.
abstract: Lesion-induced inflammatory responses in both brain and spinal cord have recently become a topic of active investigation. Using C57BL/6J mice, we compared the tissue reaction in these two central nervous system (CNS) compartments with mechanical lesions of similar size involving both grey and white matter. This evaluation included the quantitative assessment of neutrophils, lymphocytes and activated macrophages/microglia, as well as astrocyte activation, upregulation of vascular cell adhesion molecules (ICAM-1, VCAM-1, PECAM) and the extent of blood-brain barrier (BBB) breakdown. Time points analysed post-lesioning included 1, 2, 4 and 7 days (as well as 10 and 14 days for the BBB). We found clear evidence that the acute inflammatory response to traumatic injury is significantly greater in the spinal cord than in the cerebral cortex. The numbers of both neutrophils and macrophages recruited to the lesion site were significantly higher in the spinal cord than in the brain, and the recruitment of these cells into the surrounding parenchyma was also more widespread in the cord. The area of BBB breakdown was substantially larger in the spinal cord and vascular damage persisted for a longer period. In the brain, as in spinal cord, the area to which neutrophils were recruited correlated well with the area of BBB breakdown. It will be of interest to determine the extent to which the infiltration of inflammatory cells contributes, either directly or indirectly, to the vascular permeability and secondary tissue damage or, conversely, to local tissue repair in the brain and the spinal cord.
authors.affiliation: Brain Research Institute, University of Zurich, Switzerland. lschnell@hifo.unizh.ch
authors.forename: L
authors.initials: L
authors.lastname: Schnell
authors.forename: S
authors.initials: S
authors.lastname: Fearn
authors.forename: H
authors.initials: H
authors.lastname: Klassen
authors.forename: M E
authors.initials: ME
authors.lastname: Schwab
authors.forename: V H
authors.initials: VH
authors.lastname: Perry
mesh_terms: D000210:Acute-Phase Reaction / Q000276:immunology*; D000818:Animals; D001253:Astrocytes / Q000737:chemistry / Q000502:physiology; D001812:Blood-Brain Barrier / Q000502:physiology; D001921:Brain / Q000098:blood supply / Q000166:cytology / Q000276:immunology*; D004660:Encephalitis / Q000276:immunology*; D004727:Endothelium / Q000166:cytology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D006735:Horseradish Peroxidase / Q000493:pharmacokinetics; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D018655:Lymphocyte Count; D008214:Lymphocytes / Q000166:cytology / Q000276:immunology; D008264:Macrophages / Q000737:chemistry / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000737:chemistry / Q000502:physiology; D009187:Myelitis / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D013116:Spinal Cord / Q000098:blood supply / Q000166:cytology / Q000276:immunology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis
chemical_list: D005904:Glial Fibrillary Acidic Protein; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D006735:Horseradish Peroxidase