ArticleBMC molecular and cell biology2020
MazEF-rifampicin interaction suggests a mechanism for rifampicin induced inhibition of persisters.
Article in BMC molecular and cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Inhibition of efflux pumps by FDA-approved drugs oxiconazole and sertaconazole restores antibiotic susceptibility in multidrug-resistantAntimicrobial agents and chemotherapy · 2025Article
- Efflux pump modulation by Montelukast and its roles in restoring antibiotic susceptibility in multidrug-resistant Staphylococcus aureus.EBioMedicine · 2025Article
- Heterogeneous subpopulations inFrontiers in cellular and infection microbiology · 2025Article
- The ability in managing reactive oxygen species affectsmSystems · 2024Article
- Efficacy of rifampicin combination therapy against MRSA prosthetic vascular graft infections in a rat model.Biofilm · 2024Article
- Targeted Anti-Biofilm Therapy: Dissecting Targets in the Biofilm Life Cycle.Pharmaceuticals (Basel, Switzerland) · 2022Review
- MBZM-N-IBT, a Novel Small Molecule, Restricts Chikungunya Virus Infection by Targeting nsP2 Protease ActivityAntimicrobial agents and chemotherapy · 2022Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundPersistence is a natural phenomenon whereby a subset of a population of isogenic bacteria either grow slow or become dormant conferring them with the ability to withstand various stresses including antibiotics. In a clinical setting bacterial persistence often leads to the recalcitrance of various infections increasing the treatment time and cost. Additionally, some studies also indicate that persistence can also pave way for the emergence of resistant strains. In a laboratory setting this persistent phenotype is enriched in nutritionally deprived environments. Consequently, in a batch culture the late stationary phase is enriched with persistent bacteria. The mechanism of persister cell formation and its regulation is not well understood. Toxin-antitoxin (TA) systems have been implicated to be responsible for bacterial persistence and rifampicin is used to treat highly persistent bacterial strains. The current study tries to explore a possible interaction between rifampicin and the MazEF TA system that furthers the former's success rate in treating persistent bacteria.
resultsIn the current study we found that the population of bacteria in the death phase of a batch culture consists of metabolically inactive live cells resembling persisters, which showed higher membrane depolarization as compared to the log phase bacteria. We also observed an increase in the expression of the MazEF TA modules in this phase. Since rifampicin is used to kill the persisters, we assessed the interaction of rifampicin with MazEF complex. We showed that rifampicin moderately interacts with MazEF complex with 1:1 stoichiometry.
conclusionOur study suggests that the interaction of rifampicin with MazEF complex might play an important role in inhibition of persisters.
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