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微生物相互作用影响模型口腔群落的应激耐受性。

Microbial interactions impact stress tolerance in a model oral community.

机构信息

School of Biological Sciences and Center for Microbial Dynamics and Infection, Georgia Institute of Technology, Atlanta, Georgia, USA.

Emory-Children's Cystic Fibrosis Center, Atlanta, Georgia, USA.

出版信息

Microbiol Spectr. 2024 Oct 3;12(10):e0100524. doi: 10.1128/spectrum.01005-24. Epub 2024 Sep 13.

DOI:10.1128/spectrum.01005-24
PMID:39269155
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11448157/
Abstract

UNLABELLED

Understanding the molecular mechanisms governing microbial interactions is crucial for unraveling the complexities of microbial communities and their ecological impacts. Here, we employed a two-species model system comprising the oral bacteria and to investigate how synergistic and antagonistic interactions between microbes impact their resilience to environmental change and invasion by other microbes. We used an colony biofilm model and focused on two . -produced extracellular molecules, L-lactate and HO, which are known to impact fitness of this dual-species community. While the ability of to cross-feed on -produced L-lactate enhanced its fitness during co-culture, this function showed little impact on the ability of co-cultures to resist environmental change. In fact, the ability of to catabolize L-lactate may be detrimental in the presence of tetracycline, highlighting the complexity of interactions under antimicrobial stress. Furthermore, HO, known for its antimicrobial properties, had negative impacts on both species in our model system. However, HO production by enhanced tolerance to tetracycline, suggesting a protective role under antibiotic pressure. Finally, significantly inhibited the bacterium from invading biofilms, but this inhibition was lost during co-culture with and in a murine abscess model, where actually promoted invasion. These data indicate that microbial interactions can impact fitness of a bacterial community upon exposure to stresses, but these impacts are highly environment dependent.

IMPORTANCE

Microbial interactions are critical modulators of the emergence of microbial communities and their functions. However, how these interactions impact the fitness of microbes in established communities upon exposure to environmental stresses is poorly understood. Here, we utilized a two-species community consisting of and to examine the impact of synergistic and antagonistic interactions on microbial resilience to environmental fluctuations and susceptibility to microbial invasion. We focused on the -produced extracellular molecules, L-lactate and HO, which have been shown to mediate interactions between these two microbes. We discovered that seemingly beneficial functions, such as cross-feeding on -produced L-Lactate, can paradoxically exacerbate vulnerabilities, such as susceptibility to antibiotics. Moreover, our data highlight the context-dependent nature of microbial interactions, emphasizing that a seemingly potent antimicrobial, such as HO, can have both synergistic and antagonistic effects on a microbial community dependent on the environment.

摘要

未加标签

理解控制微生物相互作用的分子机制对于揭示微生物群落的复杂性及其生态影响至关重要。在这里,我们采用了包含口腔细菌 和 的两种物种模型系统,研究了微生物之间的协同和拮抗相互作用如何影响它们对环境变化和其他微生物入侵的恢复能力。我们使用了 集落生物膜模型,并专注于两种 产生的细胞外分子,L-乳酸和 HO,已知这两种分子会影响这种双物种群落的适应性。虽然 利用 产生的 L-乳酸进行交叉喂养的能力增强了其在共培养中的适应性,但这种功能对共培养物抵抗环境变化的能力几乎没有影响。事实上,在存在四环素的情况下, 代谢 L-乳酸的能力可能有害,突出了在抗菌应激下相互作用的复杂性。此外,HO 具有抗菌特性,对我们模型系统中的两种物种都有负面影响。然而, 产生的 HO 增强了 对四环素的耐受性,这表明在抗生素压力下具有保护作用。最后, 显著抑制了 细菌入侵 生物膜,但在与 共培养和在鼠脓肿模型中, 实际上促进了 的入侵,这种抑制作用消失了。这些数据表明,微生物相互作用可以影响暴露于应激下细菌群落的适应性,但这些影响高度依赖于环境。

重要性

微生物相互作用是微生物群落出现和功能的关键调节剂。然而,在暴露于环境应激时,这些相互作用如何影响已建立的群落中微生物的适应性尚不清楚。在这里,我们利用由 和 组成的两种物种群落来研究协同和拮抗相互作用对微生物对环境波动的恢复力和对微生物入侵的易感性的影响。我们专注于由 产生的细胞外分子,L-乳酸和 HO,已知它们可以调节这两种微生物之间的相互作用。我们发现,看似有益的功能,如 利用 产生的 L-乳酸进行交叉喂养,可能会产生悖论,加剧脆弱性,例如对抗生素的敏感性。此外,我们的数据突出了微生物相互作用的上下文依赖性,强调了看似有效的抗菌剂,如 HO,在依赖环境的情况下,对微生物群落可能具有协同和拮抗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/5a64d147c4e5/spectrum.01005-24.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/0b6404935b3b/spectrum.01005-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/732fbeb66b9d/spectrum.01005-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/61ceed56094b/spectrum.01005-24.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/5a64d147c4e5/spectrum.01005-24.f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/0b6404935b3b/spectrum.01005-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/732fbeb66b9d/spectrum.01005-24.f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/61ceed56094b/spectrum.01005-24.f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee21/11448157/5a64d147c4e5/spectrum.01005-24.f004.jpg

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