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首页> 外文期刊>Infection and immunity >Egg Laying Is Delayed but Worm Fecundity Is Normal in SCID Mice Infected with Schistosoma japonicum andS. mansoni with or without Recombinant Tumor Necrosis Factor Alpha Treatment
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Egg Laying Is Delayed but Worm Fecundity Is Normal in SCID Mice Infected with Schistosoma japonicum andS. mansoni with or without Recombinant Tumor Necrosis Factor Alpha Treatment

机译：感染日本血吸虫和S的SCID小鼠产卵延迟，但蠕虫繁殖力正常。曼索尼伴或不伴重组肿瘤坏死因子α治疗

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Mice with severe combined immunodeficiency (SCID mice) lack functional B and T cells. Egg laying by Schistosoma mansoniand S. japonicum was delayed in SCID mice, but in a matter of weeks worm fecundity was equivalent to that in intact mice. SCID mice formed smaller hepatic granulomas and showed less fibrosis than did intact mice. The reduction in egg-associated pathology in SCID mice correlated with marked reductions in interleukin-4 (IL-4), IL-5, IL-13, and gamma interferon mRNA expression in the liver. S. mansoni infections were frequently lethal for SCID mice infected for more than 9 weeks, while S. japonicum-infected SCID mice died at the same rate as infected intact mice. We were unable to affect hepatic granuloma formation or egg laying by worms in SCID mice by administration of recombinant murine tumor necrosis factor alpha (TNF-α). In fact, SCID and BALB/c mice appeared to express nearly equivalent levels of TNF-α mRNA in their granulomatous tissues, suggesting that there is little or no deficit in TNF-α expression in infected SCID mice. The data indicate that TNF-α may be in large part derived from a non-T-cell source. Together, these findings provide little evidence that TNF-α alone can reconstitute early fecundity, granuloma formation, or hepatic fibrosis in schistosome-infected SCID mice.
机译：患有严重合并免疫缺陷的小鼠（SCID小鼠）缺乏功能性B和T细胞。 曼氏血吸虫和 S产卵。 japonicum 在SCID小鼠中被延迟，但在几周内蠕虫的繁殖力与完整小鼠相同。与完整小鼠相比，SCID小鼠形成较小的肝肉芽肿，并显示较少的纤维化。 SCID小鼠中与卵相关的病理学降低与肝脏中白介素4（IL-4），IL-5，IL-13和γ干扰素mRNA表达的显着降低有关。 S。对于感染了9周以上的SCID小鼠，mansoni 感染经常是致命的，而 S则是。被日本血吸虫感染的SCID小鼠死亡的速度与感染的完整小鼠相同。通过施用重组鼠肿瘤坏死因子α（TNF-α），我们无法影响SCID小鼠中蠕虫引起的肝肉芽肿的形成或产卵。实际上，SCID和BALB / c小鼠似乎在其肉芽肿组织中表达几乎相等水平的TNF-αmRNA，这表明在感染的SCID小鼠中TNF-α表达几乎没有或没有缺陷。数据表明，TNF-α可能大部分来自非T细胞来源。总之，这些发现几乎没有证据表明单独的TNF-α可以重构血吸虫感染的SCID小鼠的早期生殖力，肉芽肿形成或肝纤维化。

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