Targeting Superoxide dismutase confers enhanced Reactive Oxygen Species mediated eradication of Polymyxin B induced Acinetobacter baumannii persisters

Bacterial persisters represent non-inheritable drug tolerant population that are linked to recalcitrance of infections in healthcare settings. The rise of antibiotic resistance and depletion of new antibiotics in drug discovery pipeline has made the task of persister eradication more daunting. In th...

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Published inAntimicrobial agents and chemotherapy Vol. 95; no. 5
Main Authors Dubey, Vineet, Gupta, Rinki, Pathania, Ranjana
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 19.04.2021
Subjects
Experimental Therapeutics
rifampicin
drug tolerance
drug combination
reactive oxygen species
sodB
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Abstract Bacterial persisters represent non-inheritable drug tolerant population that are linked to recalcitrance of infections in healthcare settings. The rise of antibiotic resistance and depletion of new antibiotics in drug discovery pipeline has made the task of persister eradication more daunting. In the present study, we report that treatment of with the last resort antibiotic polymyxin B displays continuous variation in tolerance among different clinical isolates. Mechanistically, Polymyxin B persisters exhibit disruption of proton motive force led delocalisation of cell division protein to attain a growth arrested phenotype. Tolerance studies on mutant strains revealed that superoxide dismutase ( ) activity is a major contributor in tolerance of to polymyxin B. Using a dual fluorescence based persister detection system, screening of various antibiotics was performed to eradicate polymyxin B induced persisters of Rifampicin exhibited eradication of polymyxin B tolerant population by log reduction of 6 in magnitude against different clinical isolates of We establish that enhanced generation of ROS by rifampicin leads to clearance of these polymyxin B persisters. It was further demonstrated, as a proof of concept, that rifampicin potentiates the killing of polymyxin B persisters in murine wound infection model. We found that the effects were linked to significant down regulation of by rifampicin, which contributes to higher generation of ROS in polymyxin B tolerant cells. In view of these results, we propose that the combination of polymyxin B and rifampicin is an effective antipersister strategy in clearing polymyxin B induced persisters.
AbstractList Bacterial persisters represent noninheritable drug-tolerant populations that are linked to recalcitrance of infections in health care settings. The rise of antibiotic resistance and the depletion of new antibiotics in the drug discovery pipeline have made the task of persister eradication more daunting. In the present study, we report that treatment of Acinetobacter baumannii with the last-resort antibiotic polymyxin B yields continuous variations in tolerance among different clinical isolates. Mechanistically, polymyxin B persisters exhibit disruption of proton motive force and delocalization of the cell division protein to attain a growth-arrested phenotype. Tolerance studies with mutant strains revealed that superoxide dismutase (sodB) activity is a major contributor to the tolerance of A. baumannii to polymyxin B. Using a dual fluorescence-based persister detection system, screening of various antibiotics to eradicate polymyxin B-induced A. baumannii persisters was performed. Rifampicin exhibited eradication of polymyxin B-tolerant populations by 6-log-unit reductions in magnitude with different clinical isolates of A. baumannii. We established that enhanced generation of reactive oxygen species (ROS) by rifampicin leads to clearance of these polymyxin B persisters. It was further demonstrated, as a proof of concept, that rifampicin potentiates the killing of polymyxin B persisters in a murine wound infection model. We found that the effects were linked to significant downregulation of sodB by rifampicin, which contributes to greater generation of ROS in polymyxin B-tolerant cells. In view of these results, we propose that the combination of polymyxin B and rifampicin is an effective antipersister strategy in clearing polymyxin B-induced A. baumannii persisters.
Bacterial persisters represent noninheritable drug-tolerant populations that are linked to recalcitrance of infections in health care settings. The rise of antibiotic resistance and the depletion of new antibiotics in the drug discovery pipeline have made the task of persister eradication more daunting. Bacterial persisters represent noninheritable drug-tolerant populations that are linked to recalcitrance of infections in health care settings. The rise of antibiotic resistance and the depletion of new antibiotics in the drug discovery pipeline have made the task of persister eradication more daunting. In the present study, we report that treatment of Acinetobacter baumannii with the last-resort antibiotic polymyxin B yields continuous variations in tolerance among different clinical isolates. Mechanistically, polymyxin B persisters exhibit disruption of proton motive force and delocalization of the cell division protein to attain a growth-arrested phenotype. Tolerance studies with mutant strains revealed that superoxide dismutase ( sodB ) activity is a major contributor to the tolerance of A. baumannii to polymyxin B. Using a dual fluorescence-based persister detection system, screening of various antibiotics to eradicate polymyxin B-induced A. baumannii persisters was performed. Rifampicin exhibited eradication of polymyxin B-tolerant populations by 6-log-unit reductions in magnitude with different clinical isolates of A. baumannii . We established that enhanced generation of reactive oxygen species (ROS) by rifampicin leads to clearance of these polymyxin B persisters. It was further demonstrated, as a proof of concept, that rifampicin potentiates the killing of polymyxin B persisters in a murine wound infection model. We found that the effects were linked to significant downregulation of sodB by rifampicin, which contributes to greater generation of ROS in polymyxin B-tolerant cells. In view of these results, we propose that the combination of polymyxin B and rifampicin is an effective antipersister strategy in clearing polymyxin B-induced A. baumannii persisters.
Bacterial persisters represent noninheritable drug-tolerant populations that are linked to recalcitrance of infections in health care settings. The rise of antibiotic resistance and the depletion of new antibiotics in the drug discovery pipeline have made the task of persister eradication more daunting. ABSTRACT Bacterial persisters represent noninheritable drug-tolerant populations that are linked to recalcitrance of infections in health care settings. The rise of antibiotic resistance and the depletion of new antibiotics in the drug discovery pipeline have made the task of persister eradication more daunting. In the present study, we report that treatment of Acinetobacter baumannii with the last-resort antibiotic polymyxin B yields continuous variations in tolerance among different clinical isolates. Mechanistically, polymyxin B persisters exhibit disruption of proton motive force and delocalization of the cell division protein to attain a growth-arrested phenotype. Tolerance studies with mutant strains revealed that superoxide dismutase ( sodB ) activity is a major contributor to the tolerance of A. baumannii to polymyxin B. Using a dual fluorescence-based persister detection system, screening of various antibiotics to eradicate polymyxin B-induced A. baumannii persisters was performed. Rifampicin exhibited eradication of polymyxin B-tolerant populations by 6-log-unit reductions in magnitude with different clinical isolates of A. baumannii . We established that enhanced generation of reactive oxygen species (ROS) by rifampicin leads to clearance of these polymyxin B persisters. It was further demonstrated, as a proof of concept, that rifampicin potentiates the killing of polymyxin B persisters in a murine wound infection model. We found that the effects were linked to significant downregulation of sodB by rifampicin, which contributes to greater generation of ROS in polymyxin B-tolerant cells. In view of these results, we propose that the combination of polymyxin B and rifampicin is an effective antipersister strategy in clearing polymyxin B-induced A. baumannii persisters.
Bacterial persisters represent non-inheritable drug tolerant population that are linked to recalcitrance of infections in healthcare settings. The rise of antibiotic resistance and depletion of new antibiotics in drug discovery pipeline has made the task of persister eradication more daunting. In the present study, we report that treatment of with the last resort antibiotic polymyxin B displays continuous variation in tolerance among different clinical isolates. Mechanistically, Polymyxin B persisters exhibit disruption of proton motive force led delocalisation of cell division protein to attain a growth arrested phenotype. Tolerance studies on mutant strains revealed that superoxide dismutase ( ) activity is a major contributor in tolerance of to polymyxin B. Using a dual fluorescence based persister detection system, screening of various antibiotics was performed to eradicate polymyxin B induced persisters of Rifampicin exhibited eradication of polymyxin B tolerant population by log reduction of 6 in magnitude against different clinical isolates of We establish that enhanced generation of ROS by rifampicin leads to clearance of these polymyxin B persisters. It was further demonstrated, as a proof of concept, that rifampicin potentiates the killing of polymyxin B persisters in murine wound infection model. We found that the effects were linked to significant down regulation of by rifampicin, which contributes to higher generation of ROS in polymyxin B tolerant cells. In view of these results, we propose that the combination of polymyxin B and rifampicin is an effective antipersister strategy in clearing polymyxin B induced persisters.
Author Gupta, Rinki
Dubey, Vineet
Pathania, Ranjana
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Keywords rifampicin
drug tolerance
drug combination
reactive oxygen species
sodB
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Citation Dubey V, Gupta R, Pathania R. 2021. Targeting superoxide dismutase confers enhanced reactive oxygen species-mediated eradication of polymyxin B-induced Acinetobacter baumannii persisters. Antimicrob Agents Chemother 65:e02180-20. https://doi.org/10.1128/AAC.02180-20.
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Snippet Bacterial persisters represent non-inheritable drug tolerant population that are linked to recalcitrance of infections in healthcare settings. The rise of...
Bacterial persisters represent noninheritable drug-tolerant populations that are linked to recalcitrance of infections in health care settings. The rise of...
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SubjectTerms Experimental Therapeutics
Title Targeting Superoxide dismutase confers enhanced Reactive Oxygen Species mediated eradication of Polymyxin B induced Acinetobacter baumannii persisters
URI https://www.ncbi.nlm.nih.gov/pubmed/33593839
https://journals.asm.org/doi/10.1128/AAC.02180-20
https://search.proquest.com/docview/2528507227
https://pubmed.ncbi.nlm.nih.gov/PMC8092903
Volume 95
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