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      Reducing bacterial antibiotic resistance by targeting bacterial metabolic pathways and disrupting RND efflux pump activity Translated title: Reducir la resistencia a los antibióticos bacterianos al dirigirse a las vías metabólicas bacterianas e interrumpir la actividad de la bomba de salida de RND

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          Abstract

          Abstract Antibiotic resistance is a significant issue for the medical community, worldwide. Many bacteria develop drug resistance by utilizing multidrug resistant or MDR efflux pumps that can export antibiotics from bacterial cells. Antibiotics are expelled from bacteria by efflux pumps a part of the resistance nodulation division (RND) family. Types of RND efflux pumps include the AcrAB-TolC tripartite protein pump. There are an excessive number of antibiotic compounds that have been discovered; however, only a few antibiotics are effective against MDR bacteria. Many bacteria become drug resistant when sharing genes that encode MDR efflux pump expression. MDR efflux pump encoding genes are incorporated into plasmids and then shared among bacteria. As a consequence, advancements in genetic engineering can sufficiently target and edit pathogenic bacterial genomes for perturbing drug resistance mechanisms. In this perspective and review, support will be provided for utilizing genetic modifications as an antimicrobial approach and tool that may effectively combat bacterial MDR. Ayhan et al. found that deleting acrB, acrA, and tolC increased the levels of antibiotic sensitivity in Escherichia coli. Researchers also found that glucose, glutamate, and fructose all induced the absorption of antibiotics by upregulating the gene expression of maeA and maeB that is a part of the MAL-pyruvate pathway. Therefore, the current perspective and review will discuss the potential efficacy of reducing antibiotic resistance by inhibiting genes that encode efflux protein pump expression while simultaneously upregulating metabolic genes for increased antibiotic uptake.

          Translated abstract

          Resumen La resistencia a los antibióticos es un problema importante para la comunidad médica en todo el mundo. Muchas bacterias desarrollan resistencia a los fármacos mediante el uso de bombas de eflujo MDR o resistentes a múltiples fármacos que pueden exportar antibióticos de las células bacterianas. Los antibióticos se expulsan de las bacterias mediante bombas de eflujo que forman parte de la familia de la división de nodulación de resistencia (RND). Los tipos de bombas de eflujo RND incluyen la bomba de proteínas tripartita AcrAB-TolC. Hay un número excesivo de compuestos antibióticos que se han descubierto; sin embargo, solo unos pocos antibióticos son eficaces contra la bacteria MDR. Muchas bacterias se vuelven resistentes a los fármacos cuando comparten genes que codifican la expresión de la bomba de eflujo MDR. Los genes que codifican la bomba de eflujo MDR se incorporan a los plásmidos y luego se comparten entre las bacterias. Como consecuencia, los avances en la ingeniería genética pueden apuntar y editar suficientemente los genomas bacterianos patógenos para perturbar los mecanismos de resistencia a los medicamentos. En esta perspectiva y revisión, se brindará apoyo para utilizar modificaciones genéticas como un enfoque y una herramienta antimicrobianos que pueden combatir eficazmente la MDR bacteriana. Ayhan y col. encontraron que la eliminación de acrB, acrA y tolC aumentaba los niveles de sensibilidad a los antibióticos en Escherichia coli. Los investigadores también encontraron que la glucosa, el glutamato y la fructosa inducían la absorción de antibióticos al regular al alza la expresión génica de maeA y maeB que es parte de la vía MAL-piruvato. Por lo tanto, la perspectiva actual y la revisión discutirán la eficacia potencial de reducir la resistencia a los antibióticos al inhibir los genes que codifican la expresión de la bomba de proteínas de salida y, al mismo tiempo, regular al alza los genes metabólicos para una mayor absorción de antibióticos.

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          Most cited references107

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          The antibiotic resistance crisis: part 1: causes and threats.

          Decades after the first patients were treated with antibiotics, bacterial infections have again become a threat because of the rapid emergence of resistant bacteria-a crisis attributed to abuse of these medications and a lack of new drug development.
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            Molecular mechanisms of antibiotic resistance.

            Antibiotic-resistant bacteria that are difficult or impossible to treat are becoming increasingly common and are causing a global health crisis. Antibiotic resistance is encoded by several genes, many of which can transfer between bacteria. New resistance mechanisms are constantly being described, and new genes and vectors of transmission are identified on a regular basis. This article reviews recent advances in our understanding of the mechanisms by which bacteria are either intrinsically resistant or acquire resistance to antibiotics, including the prevention of access to drug targets, changes in the structure and protection of antibiotic targets and the direct modification or inactivation of antibiotics.
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              Call of the wild: antibiotic resistance genes in natural environments.

              Antibiotic-resistant pathogens are profoundly important to human health, but the environmental reservoirs of resistance determinants are poorly understood. The origins of antibiotic resistance in the environment is relevant to human health because of the increasing importance of zoonotic diseases as well as the need for predicting emerging resistant pathogens. This Review explores the presence and spread of antibiotic resistance in non-agricultural, non-clinical environments and demonstrates the need for more intensive investigation on this subject.
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                Author and article information

                Journal
                ijm
                Iberoamerican Journal of Medicine
                Iberoam J Med
                Hospital San Pedro (Logroño, La Rioja, Spain )
                2695-5075
                2695-5075
                2022
                : 4
                : 1
                : 60-74
                Affiliations
                [1] orgnameIndependent Research Estados Unidos de América
                Article
                S2695-50752022000100010 S2695-5075(22)00400100010
                10.53986/ibjm.2022.0008
                37b7e965-d4c9-4d98-a5f7-5569caf7cc08

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 02 January 2022
                : 04 November 2021
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 107, Pages: 15
                Product

                SciELO Spain

                Categories
                Review

                Resistencia antibiótica,Bomba de flujo,Bacterial metabolic pathways,Antibiotic resistance,Efflux pump,Vías metabólicas bacterianas

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