共生病原体竞争影响宿主生存能力。
Commensal pathogen competition impacts host viability.
机构信息
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB T6G 2S2, Canada.
Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB T6G 2S2, Canada;
出版信息
Proc Natl Acad Sci U S A. 2018 Jul 3;115(27):7099-7104. doi: 10.1073/pnas.1802165115. Epub 2018 Jun 18.
While the structure and regulatory networks that govern type-six secretion system (T6SS) activity of are becoming increasingly clear, we know less about the role of T6SS in disease. Under laboratory conditions, uses T6SS to outcompete many Gram-negative species, including other strains and human commensal bacteria. However, the role of these interactions has not been resolved in an in vivo setting. We used the model of cholera to define the contribution of T6SS to pathogenesis. Here, we demonstrate that interactions between T6SS and host commensals impact pathogenesis. Inactivation of T6SS, or removal of commensal bacteria, attenuates disease severity. Reintroduction of the commensal, , into a germ-free host is sufficient to restore T6SS-dependent pathogenesis in which T6SS and host immune responses regulate viability. Together, our data demonstrate that T6SS acts on commensal bacteria to promote the pathogenesis of .
尽管 型分泌系统（T6SS）活性的结构和调控网络变得越来越清晰，但我们对 T6SS 在疾病中的作用知之甚少。在实验室条件下， 利用 T6SS 来与许多革兰氏阴性物种竞争，包括其他 菌株和人类共生细菌。然而，这些相互作用在体内环境中的作用尚未得到解决。我们使用 霍乱模型来定义 T6SS 对 发病机制的贡献。在这里，我们证明 T6SS 与宿主共生菌之间的相互作用会影响发病机制。T6SS 的失活或共生菌的去除会减轻疾病的严重程度。将共生菌 重新引入无菌宿主中足以恢复依赖 T6SS 的发病机制，其中 T6SS 和宿主免疫反应调节存活能力。总之，我们的数据表明 T6SS 作用于共生菌以促进 的发病机制。
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