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Ketamine intervention limits pathogen expansion in vitro

机译:氯胺酮干预限制病原体扩张体外

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摘要

Ketamine is one of several clinically important drugs whose therapeutic efficacy is due in part to their ability to act upon ion channels prevalent in nearly all biological systems. In studying eukaryotic and prokaryotic organisms in vitro, we show that ketamine short-circuits the growth and spatial expansion of three microorganisms, Stachybotrys chartarum, Staphylococcus epidermidis and Borrelia burgdorferi, at doses efficient at reducing depression-like behaviors in mouse models of clinical depression. Although our findings do not reveal the mechanism(s) by which ketamine mediates its antifungal and antibacterial effects, we hypothesize that a function of L-glutamate signal transduction is associated with the ability of ketamine to limit pathogen expansion. In general, our findings illustrate the functional similarities between fungal, bacterial and human ion channels, and suggest that ketamine or its metabolites not only act in neurons, as previously thought, but also in microbial communities colonizing human body surfaces.
机译:氯胺酮是临床上重要的药物治疗效果的部分原因他们的行动离子通道的能力几乎所有的生物系统中普遍存在。研究真核和原核生物体外,我们表明,氯胺酮短路增长和空间扩张的三个微生物、穗chartarum葡萄球菌epidermidis和包柔氏螺旋体burgdorferi,有效地减少剂量类似抑郁行为的小鼠模型临床抑郁症。揭示氯胺酮的机制(s)调节其抗真菌和抗菌影响,我们假设的一个函数L-glutamate信号转导有关与氯胺酮限制病原体的能力扩张。功能性真菌之间的相似之处,细菌和人类的离子通道,和建议氯胺酮或其代谢产物不仅在行动神经元,先前认为,但也在人体微生物群落殖民表面。

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