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Analysis of multidrug efflux transporters in resistance to fatty acid salts reveals a TolC-independent function of EmrAB in Salmonella enterica
Fatty acids salts exhibit bacteriostatic and bactericidal effects to inhibit bacterial growth and survival. Bacteria adapt to their environment to overcome these antibacterial effects through undefined mechanisms. In Gram-negative bacteria, drug efflux systems are associated with resistance to vario...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9045224/ https://www.ncbi.nlm.nih.gov/pubmed/35421142 http://dx.doi.org/10.1371/journal.pone.0266806 |
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author | Yoneda, Tomohiro Sakata, Hiroki Yamasaki, Seiji Hayashi-Nishino, Mitsuko Nishino, Kunihiko |
author_facet | Yoneda, Tomohiro Sakata, Hiroki Yamasaki, Seiji Hayashi-Nishino, Mitsuko Nishino, Kunihiko |
author_sort | Yoneda, Tomohiro |
collection | PubMed |
description | Fatty acids salts exhibit bacteriostatic and bactericidal effects to inhibit bacterial growth and survival. Bacteria adapt to their environment to overcome these antibacterial effects through undefined mechanisms. In Gram-negative bacteria, drug efflux systems are associated with resistance to various substances. Studies have identified multiple drug efflux systems in Salmonella enterica. The aim of this study was to investigate whether drug efflux systems contribute to fatty acid salts resistance in S. enterica. We used deletion and overexpressing strains of S. enterica for drug efflux transporters. Susceptibility to fatty acid salts was determined by measuring minimum inhibitory concentrations and performing growth assays. Our findings revealed that acrAB, acrEF, emrAB and tolC in S. enterica contribute resistance to fatty acid salts. Furthermore, EmrAB, which is known to function with TolC, contributes to the fatty acid salts resistance of S. enterica in a TolC-independent manner. This study revealed that drug efflux systems confer fatty acid satls resistance to S. enterica. Notably, although EmrAB is normally associated with antimicrobial resistance in a TolC-dependent manner, it was found to be involved in fatty acid salts resistance in a TolC-independent manner, indicating that the utilization of TolC by EmrAB is substrate dependent in S. enterica. |
format | Online Article Text |
id | pubmed-9045224 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-90452242022-04-28 Analysis of multidrug efflux transporters in resistance to fatty acid salts reveals a TolC-independent function of EmrAB in Salmonella enterica Yoneda, Tomohiro Sakata, Hiroki Yamasaki, Seiji Hayashi-Nishino, Mitsuko Nishino, Kunihiko PLoS One Research Article Fatty acids salts exhibit bacteriostatic and bactericidal effects to inhibit bacterial growth and survival. Bacteria adapt to their environment to overcome these antibacterial effects through undefined mechanisms. In Gram-negative bacteria, drug efflux systems are associated with resistance to various substances. Studies have identified multiple drug efflux systems in Salmonella enterica. The aim of this study was to investigate whether drug efflux systems contribute to fatty acid salts resistance in S. enterica. We used deletion and overexpressing strains of S. enterica for drug efflux transporters. Susceptibility to fatty acid salts was determined by measuring minimum inhibitory concentrations and performing growth assays. Our findings revealed that acrAB, acrEF, emrAB and tolC in S. enterica contribute resistance to fatty acid salts. Furthermore, EmrAB, which is known to function with TolC, contributes to the fatty acid salts resistance of S. enterica in a TolC-independent manner. This study revealed that drug efflux systems confer fatty acid satls resistance to S. enterica. Notably, although EmrAB is normally associated with antimicrobial resistance in a TolC-dependent manner, it was found to be involved in fatty acid salts resistance in a TolC-independent manner, indicating that the utilization of TolC by EmrAB is substrate dependent in S. enterica. Public Library of Science 2022-04-14 /pmc/articles/PMC9045224/ /pubmed/35421142 http://dx.doi.org/10.1371/journal.pone.0266806 Text en © 2022 Yoneda et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Yoneda, Tomohiro Sakata, Hiroki Yamasaki, Seiji Hayashi-Nishino, Mitsuko Nishino, Kunihiko Analysis of multidrug efflux transporters in resistance to fatty acid salts reveals a TolC-independent function of EmrAB in Salmonella enterica |
title | Analysis of multidrug efflux transporters in resistance to fatty acid
salts reveals a TolC-independent function of EmrAB in Salmonella
enterica |
title_full | Analysis of multidrug efflux transporters in resistance to fatty acid
salts reveals a TolC-independent function of EmrAB in Salmonella
enterica |
title_fullStr | Analysis of multidrug efflux transporters in resistance to fatty acid
salts reveals a TolC-independent function of EmrAB in Salmonella
enterica |
title_full_unstemmed | Analysis of multidrug efflux transporters in resistance to fatty acid
salts reveals a TolC-independent function of EmrAB in Salmonella
enterica |
title_short | Analysis of multidrug efflux transporters in resistance to fatty acid
salts reveals a TolC-independent function of EmrAB in Salmonella
enterica |
title_sort | analysis of multidrug efflux transporters in resistance to fatty acid
salts reveals a tolc-independent function of emrab in salmonella
enterica |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9045224/ https://www.ncbi.nlm.nih.gov/pubmed/35421142 http://dx.doi.org/10.1371/journal.pone.0266806 |
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