肿瘤坏死因子α是调控实验性布氏锥虫感染的关键介质。
Tumor necrosis factor alpha is a key mediator in the regulation of experimental Trypanosoma brucei infections.
作者信息
Magez S, Radwanska M, Beschin A, Sekikawa K, De Baetselier P
机构信息
Laboratory of Cellular Immunology, Flanders Interuniversity Institute for Biotechnology, Free University of Brussels (Vrije Universiteit Brussel), Brussels, Belgium.
出版信息
Infect Immun. 1999 Jun;67(6):3128-32. doi: 10.1128/IAI.67.6.3128-3132.1999.
Abstract
In order to evaluate during experimental Trypanosoma brucei infections the potential role of tumor necrosis factor alpha (TNF-alpha) in the host-parasite interrelationship, C57BL/6 TNF-alpha knockout mice (TNF-alpha-/-) as well as C57BL/6 wild-type mice were infected with pleomorphic T. brucei AnTat 1.1 E parasites. In the TNF-alpha-/- mice, the peak levels of parasitemia were strongly increased compared to the peak levels recorded in wild-type mice. The increased parasite burden did not reflect differences in clearance efficacy or in production of T. brucei-specific immunoglobulin M (IgM) and IgG antibodies. Trypanosome-mediated immunopathological features, such as lymph node-associated immunosuppression and lipopolysaccharide hypersensitivity, were found to be greatly reduced in infected TNF-alpha-/- mice. These results demonstrate that, during trypanosome infections, TNF-alpha is a key mediator involved in both parasitemia control and infection-associated pathology.
摘要
为了在实验性布氏锥虫感染期间评估肿瘤坏死因子α（TNF-α）在宿主-寄生虫相互关系中的潜在作用，将C57BL/6 TNF-α基因敲除小鼠（TNF-α-/-）以及C57BL/6野生型小鼠用多形性布氏锥虫AnTat 1.1 E寄生虫进行感染。在TNF-α-/-小鼠中，与野生型小鼠记录的峰值水平相比，寄生虫血症的峰值水平显著升高。寄生虫负担的增加并未反映出清除效率或布氏锥虫特异性免疫球蛋白M（IgM）和IgG抗体产生方面的差异。在感染的TNF-α-/-小鼠中，发现锥虫介导的免疫病理特征，如淋巴结相关免疫抑制和脂多糖超敏反应，大大降低。这些结果表明，在锥虫感染期间，TNF-α是参与寄生虫血症控制和感染相关病理的关键介质。
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