作者: D. Sun , T. A. Newman , V. H. Perry , R. O. Weller
DOI: 10.1111/J.1365-2990.2003.00546.X
关键词: Central nervous system 、 Inflammation 、 Pathology 、 Stereotaxic technique 、 Multiple sclerosis 、 Experimental autoimmune encephalomyelitis 、 Medicine 、 Microglia 、 Encephalomyelitis 、 Immunology 、 Cytokine
摘要: Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) are inflammatory diseases in which cytokines intimately involved. Here we test the hypothesis that injection of pro-inflammatory cytokines, tumour necrosis factor-? (TNF?) interferon gamma (IFN?) into brain animals prodromal phase EAE significantly enhances inflammation central nervous system (CNS). We were particularly interested to learn whether a local increase influenced pathology locally, or more extensively, within CNS. was induced female adult Lewis rats. Eight days post-inoculation, TNF? INF? injected one cerebral hemisphere. Days 11 13 post-inoculation (3 5 after cytokine) quantified by number perivascular cuffs degree major histocompatibility complex (MHC) class II expression microglia. Normal with saline served as controls. Results: microglial activation increased three- fourfold eightfold spinal cord (P ? 0.05); lymphocyte invasion sixfold 0.01) following injections compared Significant axonal damage observed white matter associated cuffs. Conclusion: changes release results widespread enhancement cord, exacerbation clinical symptoms.