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首页> 外文期刊>Infection and immunity >Tryptophan Prototrophy Contributes to Francisella tularensis Evasion of Gamma Interferon-Mediated Host Defense
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Tryptophan Prototrophy Contributes to Francisella tularensis Evasion of Gamma Interferon-Mediated Host Defense

机译：色氨酸原营养导致γ干扰素介导的宿主防御规避土拉弗朗西斯菌。

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Francisella tularensis is able to survive and replicate within host macrophages, a trait that is associated with the high virulence of this bacterium. The trpAB genes encode the enzymes required for the final two steps in tryptophan biosynthesis, with TrpB being responsible for the conversion of indole to tryptophan. Consistent with this function, an F. tularensis subsp. novicida trpB mutant is unable to grow in defined medium in the absence of tryptophan. The trpB mutant is also attenuated for virulence in a mouse pulmonary model of tularemia. However, the trpB mutant remains virulent in gamma interferon receptor-deficient (IFN-γR?/?) mice, demonstrating that IFN-γ-mediated signaling contributes to clearance of the trpB mutant. IFN-γ limits intracellular survival of the trpB mutant within bone marrow-derived macrophages from wild-type but not IFN-γR?/? mice. An F. tularensis subsp. tularensis trpB mutant is also attenuated for virulence in mice and survival within IFN-γ-treated macrophages, indicating that tryptophan prototrophy is also important in a human-virulent F. tularensis subspecies. These results demonstrate that trpB contributes to F. tularensis virulence by enabling intracellular growth under IFN-γ-mediated tryptophan limitation.
机译：图拉弗朗西斯菌能够在宿主巨噬细胞中生存和复制，这种特征与这种细菌的高毒力有关。 trpAB 基因编码色氨酸生物合成的最后两个步骤所需的酶，其中TrpB负责将吲哚转化为色氨酸。与此功能一致的是，T.ularularensis亚种。在缺少色氨酸的情况下，novicida trpB 突变体无法在指定的培养基中生长。在小鼠肺部Tularemia模型中， trpB 突变体的毒力也被减弱。但是， trpB 突变体在γ-干扰素受体缺陷型（IFN-γR？/？）小鼠中仍然具有毒性，表明IFN-γ介导的信号传导有助于清除γ-干扰素。 trpB 突变体。 IFN-γ限制了野生型小鼠骨髓来源的巨噬细胞内 trpB 突变体的细胞内存活，但没有限制IFN-γRα/β小鼠的存活。 F. tularensis亚种 tularensis trpB 突变体在小鼠中的毒力和在IFN-γ处理的巨噬细胞中的存活率也被减弱，这表明色氨酸原养型在人类致病性F. tularensis亚种中也很重要。这些结果表明 trpB 通过在IFN-γ介导的色氨酸限制下使细胞内生长而促进了图拉菌的致病性。

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