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首页> 外文期刊>Infection and immunity >High tumor necrosis factor alpha (TNF-alpha) production in Trypanosoma cruzi-infected pregnant mice and increased TNF-alpha gene transcription in their offspring.
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High tumor necrosis factor alpha (TNF-alpha) production in Trypanosoma cruzi-infected pregnant mice and increased TNF-alpha gene transcription in their offspring.

机译：在克鲁斯锥虫感染的妊娠小鼠中高肿瘤坏死因子α（TNF-alpha）的产生和其后代中TNF-alpha基因转录的增加。

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摘要

Since tumor necrosis factor alpha (TNF-alpha) is known to be involved in the feto-maternal relationship, this cytokine was studied in Trypanosoma cruzi-infected pregnant BALB/c mice and their fetuses and offspring. Pregnant chronically infected mice displayed significantly higher levels of circulating TNF-alpha than animals either only infected or only pregnant. TNF-alpha was undetectable in sera of uninfected and nonpregnant mice as well as in breast milk obtained from infected and uninfected animals. Fetuses from infected mice exhibited significantly more cells containing TNF-alpha mRNA in their thymus than fetuses from uninfected mothers. When infected 2 months after birth, offspring born to infected and uninfected mothers displayed similar amounts of circulating TNF-alpha during chronic infection, whereas this cytokine was only weakly detectable during the acute phase of the disease. An intravenous injection of lipopolysaccharide during acute infection strongly increased the production of TNF-alpha in offspring born to infected mothers to levels higher than those in progeny from uninfected mice. These results suggest that TNF-alpha is an important cytokine in the feto-maternal relationship during T. cruzi infection and that fetuses and offspring of infected mothers are primed to produce elevated levels of TNF-alpha.
机译：由于已知肿瘤坏死因子α（TNF-alpha）参与了胎儿与母亲的关系，因此在克鲁氏锥虫感染的怀孕BALB / c小鼠及其胎儿和后代中研究了这种细胞因子。与仅感染或仅怀孕的动物相比，怀孕的慢性感染的小鼠显示出显着更高的循环TNF-α水平。在未感染和未怀孕的小鼠的血清以及从感染和未感染的动物获得的母乳中，都无法检测到TNF-α。与未感染母亲的胎儿相比，来自感染小鼠的胎儿胸腺中含有更多的含有TNF-αmRNA的细胞。在出生后两个月被感染时，感染和未感染的母亲所生的后代在慢性感染期间表现出相似量的循环TNF-α，而这种细胞因子仅在疾病的急性期被弱检测到。在急性感染过程中静脉注射脂多糖可大大增加感染母亲所生后代中TNF-α的产生，使其水平高于未感染小鼠后代中的水平。这些结果表明，在克氏锥虫感染期间，TNF-α是胎儿与母体关系中的重要细胞因子，受感染母亲的胎儿和后代会被引发产生高水平的TNF-α。

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