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首页> 外文期刊>Infection and immunity >Transforming Growth Factor β-Induced Failure of Resistance to Infection with Blood-Stage Plasmodium chabaudiin Mice
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Transforming Growth Factor β-Induced Failure of Resistance to Infection with Blood-Stage Plasmodium chabaudiin Mice

机译：转化生长因子β诱导的血期查巴迪菌原性鼠抗感染失败

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The role of transforming growth factor β (TGF-β) in infection with Plasmodium chabaudi was investigated with resistant and susceptible mouse models. C57BL/10 mice produced gamma interferon (IFN-γ) and nitric oxide (NO) shortly after infection and cleared the parasite spontaneously. In contrast, BALB/c mice showed a transient enhancement of TGF-β production, followed by a relative lack of IFN-γ and NO production, and succumbed to the infection. However, there was no correlation between levels of serum TGF-β and splenic TGF-β mRNA in both mouse strains before and after infection. Administration of recombinant TGF-β (rTGF-β) rendered resistant mice susceptible because of suppression of subsequent production of IFN-γ and NO. Administration of anti-TGF-β antibody to the infected BALB/c mice resulted in remarkable increases in serum IFN-γ and NO, and the mice resisted the infection. Splenic CD4+ T and CD11b+ cells of C57BL/10 mice were significantly activated after infection, but this was completely abrogated by administration of rTGF-β. These results suggested that, in the P. chabaudi-susceptible but not resistant mice, production of TGF-β was promoted, and subsequent failure of IFN-γ- and NO-dependent resistance to the parasite was induced. This study is the first to indicate that TGF-β production was the key event in failure of resistance to mouse malaria.
机译：用耐药和易感小鼠模型研究了转化生长因子β（TGF-β）在 chabaudi 感染中的作用。 C57BL / 10小鼠在感染后不久产生了γ-干扰素（IFN-γ）和一氧化氮（NO），并自发清除了寄生虫。相反，BALB / c小鼠表现出TGF-β产生的瞬时增强，随后相对缺乏IFN-γ和NO的产生，并且死于感染。然而，在感染前后，两种小鼠品系中血清TGF-β和脾TGF-βmRNA水平之间均无相关性。重组TGF-β（rTGF-β）的给药使抗性小鼠易感，因为抑制了随后产生的IFN-γ和NO。对感染的BALB / c小鼠施用抗TGF-β抗体会导致血清IFN-γ和NO显着增加，并且小鼠抵抗感染。感染后，C57BL / 10小鼠的脾CD4 + T和CD11b + 细胞被显着激活，但通过施用rTGF-β可以完全消除。这些结果表明，在 P中。 Chabaudi易感但不耐药的小鼠，促进了TGF-β的产生，并随后诱导了IFN-γ和NO依赖的对寄生虫的耐药性衰竭。这项研究首次表明，TGF-β的产生是抵抗小鼠疟疾失败的关键事件。

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