Adaptation to bile and anaerobicity limits Vibrio cholerae phage adsorption.
Adaptation to bile and anaerobicity limits Vibrio cholerae phage adsorption.
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DOI：
10.1128/mbio.01985-23
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发表时间：
2023-12-19
期刊：
影响因子：
6.4
通讯作者：
Seed, Kimberley D.
中科院分区：
文献类型：
--
作者：
Netter, Zoe;Dunham, Drew T.;Seed, Kimberley D.
噬菌体（细菌病毒）在塑造细菌种群的进化和动态方面发挥着关键作用。细菌利用基因编码的噬菌体防御系统库，但也可以通过改变噬菌体繁殖所依赖的细胞资源的可用性来实现保护。这些生理变化通常是对独特环境信号的适应性反应。兼性病原体霍乱弧菌适应水生环境和肠道环境，具有特定生态位的生理变化，确保其在这种不同环境中的进化成功。在这两个生态位中，霍乱弧菌很容易受到 ICP1 等裂解噬菌体的捕食。然而，噬菌体和易感细菌宿主在自然界中共存，表明环境因素可能调节霍乱弧菌细胞状态以防止噬菌体感染。这项工作探索了一种响应肠道特异性胆汁和厌氧信号的修饰。我们发现在这些条件下生长的霍乱弧菌减少了其外膜脂多糖上的 O1 抗原修饰。由于 O1 抗原是 ICP1 噬菌体感染的重要组成部分，因此我们研究了部分 O1 抗原耗竭作为噬菌体防御机制的影响，并观察到 O1 耗竭限制了噬菌体吸附。我们确定了 O1 消耗的机制贡献，包括弱酸耐受系统在低 pH 下对 O1 生产的重要性，以及转录谱的改变表明 O1 生物合成资源的限制。该分析说明了肠道环境相关信号和细菌生理学之间复杂的相互作用，为霍乱弧菌提供了免受噬菌体捕食的保护。霍乱弧菌是导致霍乱的细菌病原体，霍乱是一种腹泻病，影响无法获得饮用水地区的人们。在缺乏此类基础设施的地区，霍乱占疾病爆发的很大一部分。噬菌体（噬菌体，感染细菌的病毒）由于其特异性和稳定性，最近被认为是治疗和预防霍乱等细菌性疾病爆发的潜在治疗和预防剂。这项工作研究了在肠道环境中发现的刺激背景下霍乱弧菌和噬菌体之间的相互作用，以考虑霍乱预防方案（M. Yen、L. S. Cairns 和 A. Camilli, Nat Commun 8:14187, 2017, https://doi.org/10.1038/ncomms14187）。我们发现肠道环境中的常见信号会诱导霍乱弧菌的细胞表面修饰，这也限制了一些噬菌体的结合和引发感染。这些发现可能会影响基于噬菌体的治疗设计的考虑，因为噬菌体感染似乎受到细菌对肠道环境的适应的限制。
Bacteriophages (viruses of bacteria) play a pivotal role in shaping both the evolution and dynamics of bacterial populations. Bacteria employ arsenals of genetically encoded phage defense systems, but can alternatively achieve protection by changing the availability of cellular resources that phages rely on for propagation. These physiological changes are often adaptive responses to unique environmental signals. The facultative pathogen Vibrio cholerae adapts to both aquatic and intestinal environments with niche-specific physiological changes that ensure its evolutionary success in such disparate settings. In both niches, V. cholerae is susceptible to predation by lytic phages like ICP1. However, both phages and susceptible bacterial hosts coexist in nature, indicating that environmental cues may modulate V. cholerae cell state to protect against phage infection. This work explores one such modification in response to the intestine-specific signals of bile and anaerobicity. We found that V. cholerae grown in these conditions reduces O1-antigen decoration on its outer membrane lipopolysaccharide. Because the O1-antigen is an essential moiety for ICP1 phage infection, we investigated the effect of partial O1-antigen depletion as a mechanism of phage defense and observed that O1-depletion limits phage adsorption. We identified mechanistic contributions to O1-depletion, including the essentiality of a weak acid tolerance system for O1 production at low pH and alterations in transcriptional profiles indicating limitations in resources for O1-biosynthesis. This analysis illustrates a complex interplay between signals relevant to the intestinal environment and bacterial physiology that provides V. cholerae with protection from phage predation. Vibrio cholerae is the bacterial pathogen responsible for cholera, a diarrheal disease that impacts people in areas without access to potable water. In regions that lack such infrastructure, cholera represents a large proportion of disease outbreaks. Bacteriophages (phages, viruses that infect bacteria) have recently been examined as potential therapeutic and prophylactic agents to treat and prevent bacterial disease outbreaks like cholera due to their specificity and stability. This work examines the interaction between V. cholerae and vibriophages in consideration for a cholera prophylaxis regimen (M. Yen, L. S. Cairns, and A. Camilli, Nat Commun 8:14187, 2017, https://doi.org/10.1038/ncomms14187) in the context of stimuli found in the intestinal environment. We discover that common signals in the intestinal environment induce cell surface modifications in V. cholerae that also restrict some phages from binding and initiating infection. These findings could impact considerations for the design of phage-based treatments, as phage infection appears to be limited by bacterial adaptations to the intestinal environment.
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影响因子：
14.9
作者：
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通讯作者：
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影响因子：
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作者：
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DOI：
10.1126/science.aar4120
发表时间：
2018-03-02
期刊：
Science (New York, N.Y.)
影响因子：
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影响因子：
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影响因子：
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