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双组分系统PhoP/PhoQ在对多粘菌素的固有抗性中的作用

The Role of the Two-Component System PhoP/PhoQ in Intrinsic Resistance of to Polymyxin.

作者信息

Guo Haoran, Zhao Tong, Huang Can, Chen Jingyu

机构信息

Beijing Laboratory for Food Quality and Safety, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China.

出版信息

Front Microbiol. 2022 Feb 10;13:758571. doi: 10.3389/fmicb.2022.758571. eCollection 2022.

DOI:10.3389/fmicb.2022.758571
PMID:35222323
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8867023/
Abstract

Polymyxin is the "last resort" of antibiotics. The self-induced resistance to polymyxin in Gram-negative bacteria could be mediated by lipopolysaccharide (LPS) modification, which is regulated by the two-component system, PhoP/PhoQ. is a common foodborne pathogen. However, PhoP/PhoQ has not been thoroughly studied in . In this study, the functions of PhoP/PhoQ in intrinsic resistance were investigated. The resistance of was found to decrease with the deletion of PhoP/PhoQ. Further, PhoP/PhoQ was found to play an important role in maintaining membrane permeability, intercellular metabolism, and reducing membrane depolarization. Based on subsequent studies, the binding ability of polymyxin to was decreased by the modification of LPS with structures, such as L-Ara4N and palmitate. Analysis of the gene transcription levels revealed that the LPS modification genes, and operon, were downregulated with the deletion of PhoP/PhoQ in during exposure to polymyxin. In addition, , , and were downregulated in the mutants compared with the wild-type strain. Such findings demonstrate that PhoP/PhoQ contributes to the intrinsic resistance of toward polymyxins. LPS modification with L-Ara4N or palmitate is mainly responsible for the resistance of to polymyxins. The transcription of genes related to LPS modification and PmrA/PmrB can be both affected by PhoP/PhoQ in . This study adds to current knowledge regarding the role of PhoP/PhoQ in intrinsic resistance of to polymyxin.

摘要

多粘菌素是抗生素的“最后一道防线”。革兰氏阴性菌对多粘菌素的自身诱导抗性可能由脂多糖（LPS）修饰介导，而这种修饰由双组分系统PhoP/PhoQ调控。[具体细菌名称]是一种常见的食源性病原体。然而，PhoP/PhoQ在[具体细菌名称]中尚未得到充分研究。在本研究中，对PhoP/PhoQ在[具体细菌名称]固有抗性中的功能进行了研究。发现缺失PhoP/PhoQ后，[具体细菌名称]的抗性降低。此外，还发现PhoP/PhoQ在维持膜通透性、细胞内代谢以及减少膜去极化方面发挥重要作用。基于后续研究，L - Ara4N和棕榈酸酯等结构对LPS的修饰降低了多粘菌素与[具体细菌名称]的结合能力。对基因转录水平的分析表明，在多粘菌素暴露期间，[具体细菌名称]中缺失PhoP/PhoQ会导致LPS修饰基因pmrC和pmrH - pmrF操纵子下调。此外，与野生型菌株相比，突变体中的[其他相关基因名称]也下调。这些发现表明PhoP/PhoQ有助于[具体细菌名称]对多粘菌素的固有抗性。用L - Ara4N或棕榈酸酯对LPS进行修饰是[具体细菌名称]对多粘菌素产生抗性的主要原因。PhoP/PhoQ可影响[具体细菌名称]中与LPS修饰及PmrA/PmrB相关基因的转录。本研究增加了关于PhoP/PhoQ在[具体细菌名称]对多粘菌素固有抗性中作用的现有知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/f07d68111308/fmicb-13-758571-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/13a9ca2a998f/fmicb-13-758571-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/71854ee3e6dd/fmicb-13-758571-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/a8de92de9178/fmicb-13-758571-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/f07d68111308/fmicb-13-758571-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/13a9ca2a998f/fmicb-13-758571-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/5ae45e8b9150/fmicb-13-758571-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/606dbd28d4d0/fmicb-13-758571-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/dd31add68293/fmicb-13-758571-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/71854ee3e6dd/fmicb-13-758571-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/a8de92de9178/fmicb-13-758571-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b8c6/8867023/f07d68111308/fmicb-13-758571-g007.jpg

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