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细菌遗传学方法研究感染过程中 活性氧的产生。

Bacterial Genetic Approach to the Study of Reactive Oxygen Species Production in During Infection.

机构信息

Aix-Marseille Université, CNRS, Laboratoire de Chimie Bactérienne, Institut de Microbiologie de la Méditerranée, Marseille, France.

出版信息

Front Cell Infect Microbiol. 2021 Mar 1;11:640112. doi: 10.3389/fcimb.2021.640112. eCollection 2021.

Abstract

Over the last decade, an increasing number of reports presented larvae as an important model to study host-pathogen interactions. Coherently, increasing information became available about molecular mechanisms used by this host to cope with microbial infections but few of them dealt with oxidative stress. In this work, we addressed the role of reactive oxygen species (ROS) produced by the immune system of to resist against , an intracellular pathogen responsible for a wide range of infections. We confirmed that was pathogen for and showed that it had to reach a minimal bacterial load within the hemolymph to kill the larvae. ROS production by was revealed by the virulence defects of mutants lacking catalases/peroxiredoxins or cytoplasmic superoxide dismutases, both strains being highly sensitive to these oxidants. Finally, we used bacterial transcriptional fusions to demonstrate that hydrogen peroxide (HO) was produced in the hemolymph of during infection and sensed by . In line with this observation, the HO-dependent regulator OxyR was found to be required for bacterial virulence in the larvae. These results led us to conclude that ROS production is an important mechanism used by to counteract bacterial infections and validate this host as a relevant model to study host-pathogen interactions.

摘要

在过去的十年中,越来越多的报告表明幼虫是研究宿主-病原体相互作用的重要模型。与之一致的是,越来越多的信息表明这种宿主用来应对微生物感染的分子机制,但其中很少涉及氧化应激。在这项工作中,我们研究了 产生的活性氧 (ROS) 在抵抗 的作用, 是一种负责广泛感染的细胞内病原体。我们证实 是 的病原体,并表明它必须在血淋巴中达到最低细菌负荷才能杀死幼虫。通过缺乏过氧化氢酶/过氧化物酶或细胞质超氧化物歧化酶的 突变体的毒力缺陷揭示了 的 ROS 产生,这两种菌株对这些氧化剂都非常敏感。最后,我们使用细菌转录融合来证明在感染期间 产生了过氧化氢 (HO),并且 可以感知到 。与这一观察结果一致,发现 HO 依赖性调节因子 OxyR 是幼虫中细菌毒力所必需的。这些结果使我们得出结论,ROS 的产生是 抵抗细菌感染的重要机制,并验证了该宿主作为研究宿主-病原体相互作用的相关模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c406/7957066/3ac66f130f07/fcimb-11-640112-g001.jpg

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