RecA inhibitor epicatechin prolongs the development of fluoroquinolone resistance in Pasteurella multocida.
Ciprofloxacin
Epicatechin
Pasteurella multocida
RecA inhibitors
SOS response
Journal
International journal of biological macromolecules
ISSN: 1879-0003
Titre abrégé: Int J Biol Macromol
Pays: Netherlands
ID NLM: 7909578
Informations de publication
Date de publication:
10 Nov 2023
10 Nov 2023
Historique:
received:
16
05
2023
revised:
02
11
2023
accepted:
09
11
2023
pubmed:
13
11
2023
medline:
13
11
2023
entrez:
12
11
2023
Statut:
aheadofprint
Résumé
Pasteurella multocida (P. multocida), a primary pathogen of bovine respiratory diseases, has become resistant to many antibiotics, including fluoroquinolones and aminoglycosides. A large number of studies have proved that SOS reaction plays a crucial role in the development of antibiotic resistance. We have shown that the deletion of SOS response-related genes (recA, recO) can delay the development of fluoroquinolone resistance in P. multocida, therefore, it can be used as potential targets for antibiotic resistance inhibitors. In this study, we have used molecular docking to screen RecA protein inhibitors with high throughput screening, and found that epicatechin as an inhibitor significantly inhibited the formation of fluoroquinolone resistance in P. multocida, while in vitro coadministration of epicatechin with and without ciprofloxacin improved the efficacy of the antimicrobial agent. In conclusion, our results indicate that epicatechin is an efficient RecA inhibitor, implying that combining it with ciprofloxacin is a highly promising method for treating P. multocida resistant to fluoroquinolones.
Identifiants
pubmed: 37952805
pii: S0141-8130(23)04925-5
doi: 10.1016/j.ijbiomac.2023.128026
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
128026Informations de copyright
Copyright © 2023. Published by Elsevier B.V.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.