Sternberg Jeremy M, Rodgers Jean, Bradley Barbara, Maclean Lorna, Murray Max, Kennedy Peter G E
School of Biological Sciences, Zoology Building, University of Aberdeen, Aberdeen AB24 2TZ, UK.
J Neuroimmunol. 2005 Oct;167(1-2):81-9. doi: 10.1016/j.jneuroim.2005.06.017.
The relationship of neuropathology to CNS inflammatory and counter-inflammatory cytokine production in African trypanosome-infected mice was studied using an infection model with a defined disease progression. The initial phase of CNS infection by trypanosomes, where only mild neuropathology is evident, was characterised by high levels of IL-10 and IL-6. In the later phase of CNS infection and in a post-drug treatment model, moderate to severe neuropathology was associated with high levels of IFN-gamma and TNF-alpha. The relationship of these cytokines to neuropathological grade suggests that IL-10 and IL-6 protect the CNS from inflammatory pathology when parasites first enter the brain and the data reconcile previously contradictory clinical measurements of CSF cytokines in meningoencephalitic patients with post-mortem histopathology observations.
利用具有明确疾病进展的感染模型,研究了非洲锥虫感染小鼠的神经病理学与中枢神经系统(CNS)炎性和抗炎细胞因子产生之间的关系。锥虫对中枢神经系统感染的初始阶段,仅有轻微的神经病理学表现,其特征是白细胞介素-10(IL-10)和白细胞介素-6(IL-6)水平较高。在中枢神经系统感染的后期以及药物治疗后的模型中,中度至重度神经病理学与高水平的γ干扰素(IFN-γ)和肿瘤坏死因子-α(TNF-α)相关。这些细胞因子与神经病理学分级之间的关系表明,当寄生虫首次进入大脑时,IL-10和IL-6可保护中枢神经系统免受炎性病理损害,并且这些数据使脑膜脑炎患者脑脊液细胞因子的先前矛盾的临床测量结果与死后组织病理学观察结果相吻合。