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
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
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经 6-羟基多巴胺 (6-OHDA) 处理的 C57BL/6J 小鼠中去甲肾上腺素的释放与肠道大肠杆菌中通过 QseC 组氨酸激酶受体的易位相关
DOI:
10.12659/msm.922986
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发表时间:
2020-06
影响因子:
3.1
通讯作者:
Yang Kun
中科院分区:
文献类型:
--
作者:
Meng Jun;Chen Huamei;Lv Qin;Luo Xiaodan;Yang Kun
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/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.
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