Insights into idarubicin antimicrobial activity against methicillin-resistant


Journal

Virulence
ISSN: 2150-5608
Titre abrégé: Virulence
Pays: United States
ID NLM: 101531386

Informations de publication

Date de publication:
01 01 2020
Historique:
pubmed: 20 5 2020
medline: 13 7 2021
entrez: 20 5 2020
Statut: ppublish

Résumé

MRSA is a major concern in community settings and in health care. The emergence of biofilms and persister cells substantially increases its antimicrobial resistance. It is very urgent to develop new antimicrobials to solve this problem. Idarubicin was profiled to assess its antimicrobial effects We investigated the antimicrobial effects of idarubicin against MRSA by time-kill analysis. The antibiofilm efficacy of idarubicin was assessed by crystal violet and XTT staining, followed by laser confocal microscopy observation. The mechanisms underlying the antimicrobial effects were studied by transmission electron microscopy, all-atom molecular dynamic simulations, SYTOX staining, surface plasma resonance, and DNA gyrase inhibition assay. Further, we addressed the antimicrobial efficacy in wound and subcutaneous abscess infection Idarubicin kills MRSA cells by disrupting the lipid bilayers and interrupting the DNA topoisomerase IIA subunits, and idarubicin shows synergistic antimicrobial effects with fosfomycin. Through synergy with a single dose treatment fosfomycin and the addition of the cell protector amifostine, the cytotoxicity and cardiotoxicity of idarubicin were significantly reduced without affecting its antimicrobial effects. Idarubicin alone or in combination with fosfomycin exhibited considerable efficacy in a subcutaneous abscess mouse model of MRSA infection. In addition, idarubicin also showed a low probability of causing resistance and good postantibiotic effects. Idarubicin and its analogs have the potential to become a new class of antimicrobials for the treatment of MRSA-related infections.

Sections du résumé

BACKGROUND
MRSA is a major concern in community settings and in health care. The emergence of biofilms and persister cells substantially increases its antimicrobial resistance. It is very urgent to develop new antimicrobials to solve this problem.
OBJECTIVE
Idarubicin was profiled to assess its antimicrobial effects
METHODS
We investigated the antimicrobial effects of idarubicin against MRSA by time-kill analysis. The antibiofilm efficacy of idarubicin was assessed by crystal violet and XTT staining, followed by laser confocal microscopy observation. The mechanisms underlying the antimicrobial effects were studied by transmission electron microscopy, all-atom molecular dynamic simulations, SYTOX staining, surface plasma resonance, and DNA gyrase inhibition assay. Further, we addressed the antimicrobial efficacy in wound and subcutaneous abscess infection
RESULTS
Idarubicin kills MRSA cells by disrupting the lipid bilayers and interrupting the DNA topoisomerase IIA subunits, and idarubicin shows synergistic antimicrobial effects with fosfomycin. Through synergy with a single dose treatment fosfomycin and the addition of the cell protector amifostine, the cytotoxicity and cardiotoxicity of idarubicin were significantly reduced without affecting its antimicrobial effects. Idarubicin alone or in combination with fosfomycin exhibited considerable efficacy in a subcutaneous abscess mouse model of MRSA infection. In addition, idarubicin also showed a low probability of causing resistance and good postantibiotic effects.
CONCLUSIONS
Idarubicin and its analogs have the potential to become a new class of antimicrobials for the treatment of MRSA-related infections.

Identifiants

pubmed: 32423280
doi: 10.1080/21505594.2020.1770493
pmc: PMC7549941
doi:

Substances chimiques

Anti-Bacterial Agents 0
Fosfomycin 2N81MY12TE
Idarubicin ZRP63D75JW

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

636-651

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Auteurs

Pengfei She (P)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Shijia Li (S)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Linying Zhou (L)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Zhen Luo (Z)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Jinfeng Liao (J)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Lanlan Xu (L)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Xianghai Zeng (X)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Ti Chen (T)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Yaqian Liu (Y)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

Yong Wu (Y)

Department of Clinical Laboratory, The Third Xiangya Hospital of Central South University , Changsha, R.P. China.

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Classifications MeSH