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LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli

Mammary pathogenic Escherichia coli (MPEC) is an important causative agent of mastitis in dairy cows that results in reduced milk quality and production, and is responsible for severe economic losses in the dairy industry worldwide. Oxidative stress, as an imbalance between reactive oxygen species (...

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Autores principales: Wang, Hui, Shang, Fei, Shen, Jiawei, Xu, Jingyi, Chen, Xiaolin, Ni, Jingtian, Yu, Lumin, Xue, Ting
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8487509/
https://www.ncbi.nlm.nih.gov/pubmed/34600565
http://dx.doi.org/10.1186/s13567-021-00998-8
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author Wang, Hui
Shang, Fei
Shen, Jiawei
Xu, Jingyi
Chen, Xiaolin
Ni, Jingtian
Yu, Lumin
Xue, Ting
author_facet Wang, Hui
Shang, Fei
Shen, Jiawei
Xu, Jingyi
Chen, Xiaolin
Ni, Jingtian
Yu, Lumin
Xue, Ting
author_sort Wang, Hui
collection PubMed
description Mammary pathogenic Escherichia coli (MPEC) is an important causative agent of mastitis in dairy cows that results in reduced milk quality and production, and is responsible for severe economic losses in the dairy industry worldwide. Oxidative stress, as an imbalance between reactive oxygen species (ROS) and antioxidants, is a stress factor that is common in most bacterial habitats. The presence of ROS can damage cellular sites, including iron-sulfur clusters, cysteine and methionine protein residues, and DNA, and may cause bacterial cell death. Previous studies have reported that Autoinducer 2 (AI-2) can regulate E. coli antibiotic resistance and pathogenicity by mediating the intracellular receptor protein LsrR. This study explored the regulatory mechanism of LsrR on the H(2)O(2) stress response in MPEC, showing that the transcript levels of lsrR significantly decreased under H(2)O(2) stress conditions. The survival cell count of lsrR mutant XW10/pSTV28 was increased about 3080-fold when compared with that of the wild-type WT/pSTV28 in the presence of H(2)O(2) and overexpression of lsrR (XW10/pUClsrR) resulted in a decrease in bacterial survival rates under these conditions. The β-galactosidase reporter assays showed that mutation of lsrR led to a remarkable increase in expression of the promoters of ahpCF, katG and oxyR, while lsrR-overexpressing significantly reduced the expression of ahpCF and katG. The electrophoretic mobility shift assays confirmed that LsrR could directly bind to the promoter regions of ahpCF and katG. These results revealed the important role played by LsrR in the oxidative stress response of MPEC.
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spelling pubmed-84875092021-10-04 LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli Wang, Hui Shang, Fei Shen, Jiawei Xu, Jingyi Chen, Xiaolin Ni, Jingtian Yu, Lumin Xue, Ting Vet Res Research Article Mammary pathogenic Escherichia coli (MPEC) is an important causative agent of mastitis in dairy cows that results in reduced milk quality and production, and is responsible for severe economic losses in the dairy industry worldwide. Oxidative stress, as an imbalance between reactive oxygen species (ROS) and antioxidants, is a stress factor that is common in most bacterial habitats. The presence of ROS can damage cellular sites, including iron-sulfur clusters, cysteine and methionine protein residues, and DNA, and may cause bacterial cell death. Previous studies have reported that Autoinducer 2 (AI-2) can regulate E. coli antibiotic resistance and pathogenicity by mediating the intracellular receptor protein LsrR. This study explored the regulatory mechanism of LsrR on the H(2)O(2) stress response in MPEC, showing that the transcript levels of lsrR significantly decreased under H(2)O(2) stress conditions. The survival cell count of lsrR mutant XW10/pSTV28 was increased about 3080-fold when compared with that of the wild-type WT/pSTV28 in the presence of H(2)O(2) and overexpression of lsrR (XW10/pUClsrR) resulted in a decrease in bacterial survival rates under these conditions. The β-galactosidase reporter assays showed that mutation of lsrR led to a remarkable increase in expression of the promoters of ahpCF, katG and oxyR, while lsrR-overexpressing significantly reduced the expression of ahpCF and katG. The electrophoretic mobility shift assays confirmed that LsrR could directly bind to the promoter regions of ahpCF and katG. These results revealed the important role played by LsrR in the oxidative stress response of MPEC. BioMed Central 2021-10-02 2021 /pmc/articles/PMC8487509/ /pubmed/34600565 http://dx.doi.org/10.1186/s13567-021-00998-8 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Wang, Hui
Shang, Fei
Shen, Jiawei
Xu, Jingyi
Chen, Xiaolin
Ni, Jingtian
Yu, Lumin
Xue, Ting
LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli
title LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli
title_full LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli
title_fullStr LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli
title_full_unstemmed LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli
title_short LsrR, the effector of AI-2 quorum sensing, is vital for the H(2)O(2) stress response in mammary pathogenic Escherichia coli
title_sort lsrr, the effector of ai-2 quorum sensing, is vital for the h(2)o(2) stress response in mammary pathogenic escherichia coli
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8487509/
https://www.ncbi.nlm.nih.gov/pubmed/34600565
http://dx.doi.org/10.1186/s13567-021-00998-8
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