An enteric virus can replace the beneficial function of commensal bacteria.

An enteric virus can replace the beneficial function of commensal bacteria.
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DOI:
10.1038/nature13960
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发表时间:
2014-12-04
期刊:
影响因子:
64.8
通讯作者:
Cadwell, Ken
Cadwell, Ken
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Kernbauer, Elisabeth;Ding, Yi;Cadwell, Ken

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肠道微生物群落对宿主生理有深远的影响。虽然共生细菌的共生作用已经得到了很好的证实,但在稳态条件下存在于胃肠道中的真核病毒的作用尚不明确。在这里,我们证明了一种常见的肠道RNA病毒可以取代肠道中共生细菌的有益功能。小鼠诺如病毒(MNV)感染无菌或抗生素处理的小鼠恢复肠道形态和淋巴细胞功能,而不引起明显的炎症和疾病。MNV的存在还抑制了在没有细菌的情况下观察到的2组先天淋巴样细胞(ILCs)的扩增,并诱导了肠道中与免疫发育和I型干扰素(IFN)信号传导相关的转录变化。与这一观察结果一致,IFNα受体对于MNV补偿细菌损耗的能力至关重要。重要的是,在肠道损伤和致病性细菌感染模型中,MNV感染抵消了抗生素治疗的有害作用。这些数据表明真核病毒具有支持肠道稳态和形成粘膜免疫的能力,类似于共生细菌。
Intestinal microbial communities have profound effects on host physiology. Whereas the symbiotic contribution of commensal bacteria is well established, the role of eukaryotic viruses that are present in the gastrointestinal tract under homeostatic conditions is undefined. Here, we demonstrate that a common enteric RNA virus can replace the beneficial function of commensal bacteria in the intestine. Murine norovirus (MNV) infection of germfree or antibiotics-treated mice restored intestinal morphology and lymphocyte function without inducing overt inflammation and disease. The presence of MNV also suppressed an expansion of group 2 innate lymphoid cells (ILCs) observed in the absence of bacteria, and induced transcriptional changes in the intestine associated with immune development and type I interferon (IFN) signaling. Consistent with this observation, the IFNα receptor was essential for the ability of MNV to compensate for bacterial depletion. Importantly, MNV infection offset the deleterious effect of antibiotics-treatment in models of intestinal injury and pathogenic bacterial infection. These data indicate that eukaryotic viruses have the capacity to support intestinal homeostasis and shape mucosal immunity akin to commensal bacteria.
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