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通过在小鼠肠道中积累乙酸来实现对碳青霉烯类耐药 的去殖民化。

Anticolonization of Carbapenem-Resistant by LP1812 Through Accumulated Acetic Acid in Mice Intestinal.

机构信息

Department of Critical Care Medicine, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Key Laboratory of Microbial Technology and Bioinformatics of Zhejiang Province, Sir Run Run Shaw Hospital, Hangzhou, China.

出版信息

Front Cell Infect Microbiol. 2021 Dec 15;11:804253. doi: 10.3389/fcimb.2021.804253. eCollection 2021.

Abstract

Carbapenem-resistant (CRKP) is highly prevalent and poses a significant threat to public health. In critically ill patients, gut colonization is considered to be the reservoir of recurrent CRKP infection. Therefore, eliminating CRKP carriage in the intestine is critical for preventing subsequent CRKP infection. In the present study, LP1812, a probiotic that can inhibit CRKP , was used as a candidate probiotic to investigate its efficacy for CRKP anticolonization. Compared with the control, mice fed with 1×10 CFU LP1812 exhibited significant CRKP clearance from 1×10 CFU/mg to less than 10 CFU/mg in mice feces. Furthermore, 16S RNA gene sequencing revealed that LP1812 modulated mice microbiota by increasing the relative abundance of the genus , , and . Further KEGG pathway enrichment analysis revealed that fatty acid-utilizing bacteria, such as acetate-producing and flourished in mice fed with LP1812. Moreover, we found that the concentration of acetic acid was higher in LP1812, which inhibited the growth of strains . Meanwhile, mice intragastrically administered with acetic acid exhibited significantly increased CRKP elimination . In conclusion, LP1812 is a potential candidate for intestinal CRKP anticolonization by regulating the intestinal microbiota and inhibiting CRKP increased acetic acid in the intestinal lumen.

摘要

耐碳青霉烯肠杆菌(CRKP)的流行率很高,对公共健康构成重大威胁。在危重症患者中,肠道定植被认为是反复发生 CRKP 感染的储库。因此,消除肠道中的 CRKP 定植对于预防随后的 CRKP 感染至关重要。在本研究中,使用 LP1812 作为候选益生菌,它是一种可以抑制 CRKP 的益生菌,来研究其抑制 CRKP 定植的效果。与对照组相比,喂食 1×10 CFU LP1812 的小鼠从 1×10 CFU/mg 到小于 10 CFU/mg 的粪便中明显清除了 CRKP。此外,16S RNA 基因测序表明,LP1812 通过增加属的相对丰度来调节小鼠的微生物群, 和 。进一步的 KEGG 途径富集分析表明,在喂食 LP1812 的小鼠中,利用脂肪酸的细菌,如产生乙酸盐的 和 大量繁殖。此外,我们发现 LP1812 中的乙酸浓度较高,抑制了 菌株的生长。同时,经灌胃给予乙酸的小鼠中 CRKP 的消除明显增加。总之,LP1812 通过调节肠道微生物群并抑制肠道腔中 CRKP 增加的乙酸来抑制肠道 CRKP 定植,是一种潜在的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/feef/8714838/8bd5707bbab3/fcimb-11-804253-g001.jpg

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