Abstract
Bacterial multidrug efflux pumps are antibiotic resistance determinants present in all microorganisms. With few exceptions, they are chromosomally encoded and present a conserved organization both at the genetic and at the protein levels. In addition, most, if not all, strains of a given bacterial species present the same chromosomally-encoded efflux pumps. Altogether this indicates that multidrug efflux pumps are ancient elements encoded in bacterial genomes long before the recent use of antibiotics for human and animal therapy. In this regard, it is worth mentioning that efflux pumps can extrude a wide range of substrates that include, besides antibiotics, heavy metals, organic pollutants, plant-produced compounds, quorum sensing signals or bacterial metabolites, among others. In the current review, we present information on the different functions that multidrug efflux pumps may have for the bacterial behaviour in different habitats as well as on their regulation by specific signals. Since, in addition to their function in non-clinical ecosystems, multidrug efflux pumps contribute to intrinsic, acquired, and phenotypic resistance of bacterial pathogens, the review also presents information on the search for inhibitors of multidrug efflux pumps, which are currently under development, in the aim of increasing the susceptibility of bacterial pathogens to antibiotics.
Highlights
Resistance to antibiotics can be explained in biochemical terms as the inability of a given antibiotic to reach its microbial target at an adequate concentration for inhibiting the target's activity
The presence of MDR efflux pumps in bacteria is not restricted to clinical environments, which are characterized by the presence of high levels of antibiotics
These results indicate that bacterial efflux pumps, in addition to being antibiotic resistance determinants, are relevant elements for the physiology of microorganisms in natural ecosystems, in the cases above described in bacteria/plant interactions
Summary
Resistance to antibiotics can be explained in biochemical terms as the inability of a given antibiotic to reach its microbial target at an adequate concentration for inhibiting the target's activity Within this scope, there are two main ways of acquiring resistance: decreasing the affinity of the target for the antibiotic (mutations in genes encoding the antimicrobial targets) or diminishing the active concentration of the antibiotic inside the cell. The acquisition of resistance to multiple antimicrobials is the consequence of the presence in the same genetic mobile element of several genes, each one encoding a different resistance. The acquisition of resistance to multiple antimicrobials is the consequence of the presence in the same genetic mobile element of several genes, each one encoding a different resistance ddeetteerrmmiinnaanntt((ccoo--rreessiissttaannccee).).HHoowweevveer,r,ininsosommeeococcacsaisoinosnsthtehesasmame deedteetremrminiannatnctacnacnocnofenrferersriesstaisntcaenctoe dtoiffderieffnetreannttimanictrimobiicarlosb(icarlosss(-crreosissst-arnescies)t.aTnhcee)m. CThhaersaectechriasrtaiccstesruisgtgicesststuhgagt etshte trhoalet otfhefflruolxepoufmepfsflausxrepluevmapnst aanstibreioletivcarnetsiastnatnibcieotdiceterremsiisntaannctes idnetbearcmteirniaanl tpsaitnhobgacetnesriiaslapraethceongteenvseins ta, lriekceelnytseevceonntd, alirkyeltyo soetchoenrdfuarnyctioonotahl errolfeusnwctitohnarel lreovlaesncweitoh brealcetvearinaclephtoysbioalcotgeyria[3l,2p1h,2y2s]i.oSloogmye[o3f,2t1h,e2s2e].fuSnocmtieonoafl rtohleessenfoutndcitrieocntlayl lrinokleesdntotandtiirbeicottliyc rleinsiksetadnctoe arnetidbisoctuicssredsisbtealnocwe.are discussed below
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