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Fast bacterial growth reduces antibiotic accumulation and efficacy.
Lapinska, Urszula; Voliotis, Margaritis; Lee, Ka Kiu; Campey, Adrian; Stone, M Rhia L; Tuck, Brandon; Phetsang, Wanida; Zhang, Bing; Tsaneva-Atanasova, Krasimira; Blaskovich, Mark A T; Pagliara, Stefano.
Afiliación
  • Lapinska U; Living Systems Institute, University of Exeter, Exeter, United Kingdom.
  • Voliotis M; Biosciences, University of Exeter, Exeter, United Kingdom.
  • Lee KK; Living Systems Institute, University of Exeter, Exeter, United Kingdom.
  • Campey A; Department of Mathematics, University of Exeter, Exeter, United Kingdom.
  • Stone MRL; Living Systems Institute, University of Exeter, Exeter, United Kingdom.
  • Tuck B; Biosciences, University of Exeter, Exeter, United Kingdom.
  • Phetsang W; Living Systems Institute, University of Exeter, Exeter, United Kingdom.
  • Zhang B; Biosciences, University of Exeter, Exeter, United Kingdom.
  • Tsaneva-Atanasova K; Centre for Superbug Solutions, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
  • Blaskovich MAT; Department of Chemistry and Chemical Biology, Rutgers, the State University of New Jersey, Piscataway, United States.
  • Pagliara S; Living Systems Institute, University of Exeter, Exeter, United Kingdom.
Elife ; 112022 06 07.
Article en En | MEDLINE | ID: mdl-35670099
Bacteria can cause an array of diseases ranging from mildly inconvenient to deadly. In fact, every year around the world, five million people succumb to a bacterial infection. Antibiotics can kill bacteria or stop their growth, but many bacterial species are now able to evade these drugs. To be efficient, most antibiotics first need to get inside a bacterium; there, they accumulate until they reach the concentration they need to act. Often, the drugs make their way through channel-like structures ('pores') studded through the external membranes of bacteria and which control the passage of molecules in and out of cells. Resistance usually emerges when genetic changes provide the microorganism with an advantage against antibiotics, or when the microorganism performs the biochemical reactions necessary for life at a slower pace. In contrast, Lapinska, Pagliara et al. decided to examine how genetically similar Escherichia coli bacteria which differed in their growth rate would fare against antibiotics. The drug targeted ribosomes, the machinery that produces proteins in a cell. A combination of techniques was used to follow individual cells, revealing that fast-growing variants better managed to survive. A closer look showed that bacteria which were growing quickly had a surplus of ribosomes, which then produced more pores that could pump the antibiotic out the cell. Next, Lapinska, Pagliara et al. exposed the bacteria to both the antibiotic and a compound that weakens bacterial membrane; this erased the advantage shown by the fast-growing variants. Overall, this work gives a finer understanding of the mechanisms that underlie antibiotic resistance, which could help pave the way to new strategies to combat harmful bacteria.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas de Escherichia coli / Antibacterianos Tipo de estudio: Prognostic_studies Idioma: En Revista: Elife Año: 2022 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Proteínas de Escherichia coli / Antibacterianos Tipo de estudio: Prognostic_studies Idioma: En Revista: Elife Año: 2022 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Reino Unido