Cytokine‐induced enhancement of autoimmune inflammation in the brain and spinal cord: implications for multiple sclerosis

Neuropathology and Applied Neurobiology - Tập 30 Số 4 - Trang 374-384 - 2004
Dong Sun1,2, Tracey A. Newman3,2, V. Hugh Perry3, Roy O. Weller2
1Current address: Medical College of Virginia, Virginia Commonwealth University, Richmond, VA, USA.
2Pathology and Clinical Neurosciences (Neuropathology), and
3CNS Inflammation Group, University of Southampton, Southampton, UK

Tóm tắt

Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) are autoimmune inflammatory diseases in which cytokines are intimately involved. Here we test the hypothesis that injection of pro‐inflammatory cytokines, tumour necrosis factor‐α (TNFα) and interferon gamma (IFNγ) into the brain of animals in the prodromal phase of EAE significantly enhances inflammation in the central nervous system (CNS). We were particularly interested to learn whether a local increase in cytokines influenced the pathology locally, or more extensively, within the CNS. EAE was induced in female adult Lewis rats. Eight days post‐inoculation, TNFα or INFγ was injected into one cerebral hemisphere. Days 11 and 13 post‐inoculation (3 and 5 days after the injection of cytokine) inflammation was quantified by the number of perivascular cuffs and the degree of major histocompatibility complex (MHC) class II expression by microglia. Normal animals injected with cytokines, and EAE animals with saline injection served as controls. Results: microglial activation was increased three‐ to fourfold in the brain and eightfold in the spinal cord (P ≤ 0.05); lymphocyte invasion was increased sixfold in the brain and three‐ to fourfold in the spinal cord (P ≤ 0.01) following injections of TNFα or INFγ in EAE animals compared with controls. Significant axonal damage was observed in white matter associated with the perivascular cuffs. Conclusion: local changes in the release of pro‐inflammatory cytokines within the brain in EAE results in the widespread enhancement of autoimmune inflammation within the brain and cord, and exacerbation of clinical symptoms.

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