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细菌移位可增加血浆皮质酮以及脑儿茶酚胺和吲哚胺的代谢。

Bacterial translocation can increase plasma corticosterone and brain catecholamine and indoleamine metabolism.

作者信息

Ando T, Brown R F, Berg R D, Dunn A J

机构信息

Department of Pharmacology and Therapeutics, Louisiana State University Medical Center, Shreveport, Louisiana 71130, USA.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2000 Dec;279(6):R2164-72. doi: 10.1152/ajpregu.2000.279.6.R2164.

DOI:10.1152/ajpregu.2000.279.6.R2164
PMID:11080082
Abstract

The potential contribution of stress-induced bacterial translocation to the activation of the hypothalamo-pituitary-adrenocortical (HPA) axis and brain biogenic amines was assessed. Mice were restrained for various periods, and brain concentrations of tryptophan, catecholamines, serotonin, and their metabolites, plasma corticosterone, and the translocation of viable bacteria from the gastrointestinal tract to the mesenteric lymph nodes, spleen, and liver were measured. Restraint induced the translocation of indigenous gram-positive bacteria in only a small proportion of animals, but translocation of gram-negative bacteria did not occur. Restraint induced short-lived increases in plasma corticosterone and brain amine metabolism, whereas bacterial translocation was slower and persisted long after the HPA axis and neurochemical responses had dissipated. When mice were infected with Salmonella typhimurium, spontaneous translocation occurred and plasma corticosterone, interleukin-6 concentrations, and brain catecholamine and indoleamine metabolism were elevated. These findings indicate that the translocation of indigenous gastrointestinal bacteria did not contribute to the HPA axis and neurochemical changes induced by restraint. However, translocation of nonindigenous S. typhimurium with or without restraint did induce HPA and neurochemical responses.

摘要

评估了应激诱导的细菌移位对下丘脑 - 垂体 - 肾上腺皮质(HPA)轴激活和脑内生物胺的潜在作用。对小鼠进行不同时间段的束缚,并测量脑内色氨酸、儿茶酚胺、5-羟色胺及其代谢产物的浓度、血浆皮质酮以及活细菌从胃肠道向肠系膜淋巴结、脾脏和肝脏的移位情况。束缚仅在一小部分动物中诱导了本土革兰氏阳性菌的移位,但未发生革兰氏阴性菌的移位。束缚诱导血浆皮质酮和脑胺代谢出现短暂升高,而细菌移位较慢且在HPA轴和神经化学反应消退后仍持续很长时间。当小鼠感染鼠伤寒沙门氏菌时,发生了自发性移位,且血浆皮质酮、白细胞介素-6浓度以及脑儿茶酚胺和吲哚胺代谢均升高。这些发现表明,本土胃肠道细菌的移位对束缚诱导的HPA轴和神经化学变化没有作用。然而,无论有无束缚,非本土鼠伤寒沙门氏菌的移位确实诱导了HPA和神经化学应答。

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