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6-羟多巴胺(6-OHDA)处理的 C57BL/6J 小鼠中去甲肾上腺素的释放与肠大肠杆菌中的转位有关,通过 QseC 组氨酸激酶受体。

The Release of Norepinephrine in C57BL/6J Mice Treated with 6-Hydroxydopamine (6-OHDA) is Associated with Translocations in Enteric Escherichia coli via the QseC Histidine Kinase Receptor.

机构信息

Department of Cardiovascular Surgery, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China (mainland).

Department of Anesthesiology, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China (mainland).

出版信息

Med Sci Monit. 2020 Aug 7;26:e922986. doi: 10.12659/MSM.922986.

DOI:10.12659/MSM.922986
PMID:32764532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7433386/
Abstract

BACKGROUND We aimed to investigate the effects of norepinephrine (NE) released from endogenous stores on bacterial translocation of Escherichia coli in mice by administration of 6-hydroxydopamine (6-OHDA), which selectively destroys noradrenergic nerve terminals. MATERIAL AND METHODS E. coli strain BW25113 and its derivatives (BW25113ΔqseC and BW25113ΔqseC pQseC) were used in this study. The serum concentrations of endotoxin were analyzed. The strains BW25113, BW25113ΔqseC, and BW25113ΔqseC pQseC were detected respectively in tissue specimens harvested from mice treated with 6-OHDA. RESULTS Mice treated with BW25113ΔqseC showed reduced levels of bacterial translocation following administration of 6-OHDA compared with mice treated with BW25113. The defect of E. coli QseC receptor caused the norepinephrine-QseC signal chain to be interrupted, and the invasiveness and penetrating power of the bacteria on the intestinal mucosa was weakened, eventually leading to a significant decrease in the incidence of bacterial translocation. CONCLUSIONS NE modulates the interaction of enteric bacterial pathogens with their hosts via QseC. The blockade of the QseC receptor-mediated effects may be useful to attenuate bacterial translocation.

摘要

背景

我们旨在通过给予 6-羟多巴胺(6-OHDA)来研究内源性储存的去甲肾上腺素(NE)对小鼠大肠杆菌细菌易位的影响,6-OHDA 可选择性地破坏去甲肾上腺素能神经末梢。

材料与方法

本研究使用了大肠杆菌 BW25113 及其衍生物(BW25113ΔqseC 和 BW25113ΔqseC pQseC)。分析了血清内毒素浓度。在接受 6-OHDA 治疗的小鼠组织标本中检测了 BW25113、BW25113ΔqseC 和 BW25113ΔqseC pQseC 这三种菌株。

结果

与接受 BW25113 治疗的小鼠相比,接受 BW25113ΔqseC 治疗的小鼠在给予 6-OHDA 后细菌易位水平降低。大肠杆菌 QseC 受体的缺陷导致去甲肾上腺素-QseC 信号链被中断,细菌对肠黏膜的侵袭力和穿透力减弱,最终导致细菌易位的发生率显著降低。

结论

NE 通过 QseC 调节肠道细菌病原体与其宿主的相互作用。阻断 QseC 受体介导的作用可能有助于减轻细菌易位。

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本文引用的文献

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Auton Neurosci. 2019 Nov;221:102584. doi: 10.1016/j.autneu.2019.102584. Epub 2019 Aug 24.
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FXR modulates the gut-vascular barrier by regulating the entry sites for bacterial translocation in experimental cirrhosis.FXR 通过调节实验性肝硬化中细菌易位的进入部位来调节肠道-血管屏障。
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QseC Signaling in the Outbreak O104:H4 Strain Combines Multiple Factors during Infection.
爆发性 O104:H4 菌株中 QseC 信号的作用在感染过程中结合了多种因素。
J Bacteriol. 2019 Aug 8;201(17). doi: 10.1128/JB.00203-19. Print 2019 Sep 1.
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Gastrointestinal non-motor dysfunction in Parkinson's disease model rats with 6-hydroxydopamine.帕金森病 6-羟多巴胺模型大鼠的胃肠道非运动功能障碍。
Physiol Res. 2019 Apr 30;68(2):295-303. doi: 10.33549/physiolres.933995. Epub 2019 Jan 10.
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Polyphenols-gut microbiota interplay and brain neuromodulation.多酚-肠道微生物群的相互作用与大脑神经调节
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A Simple Gut Model for Studying the Interaction between Escherichia coli and the Intestinal Commensal Microbiota in Cecal Mucus.一种简单的肠道模型,用于研究大肠杆菌与盲肠黏液中肠道共生菌群的相互作用。
Appl Environ Microbiol. 2018 Nov 30;84(24). doi: 10.1128/AEM.02166-18. Print 2018 Dec 15.
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Gut microbiota regulates mouse behaviors through glucocorticoid receptor pathway genes in the hippocampus.肠道微生物群通过海马中的糖皮质激素受体途径基因调节小鼠行为。
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