Cibler l’accumulation de polyp chez E. coli à l’aide d’inhibiteurs de PPK pour perturber les mécanismes de résistance aux antibiotiques

Auteurs-es

  • Benejah Moleko University of Ottawa, Ottawa, ON, Canada
  • Elizabeth Tsyben University of Ottawa, Ottawa, ON, Canada
  • Michael Downey University of Ottawa, Ottawa, ON, Canada

DOI :

https://doi.org/10.18192/osurj.v5i2.8075

Résumé

Les polyphosphates (polyP) sont des chaînes linéaires de phosphate inorganique (Pi) hautement conservées chez divers organismes. Chez Escherichia coli, le PolyP est synthétisé principalement par la polyphosphate kinase 1 (PPK1, codée par ppk) en réponse aux facteurs de stress environnementaux. Le PolyP contribue à la survie bactérienne en régulant la formation de biofilms, les réponses au stress et la résistance aux antibiotiques. Les mécanismes contrôlant l’accumulation de polyP et leurs effets sur la physiologie et la résistance bactériennes restent incomplètement compris. Notamment, l’accumulation de polyP médiée par PPK module la structure des lipopolysaccharides (LPS), contribuant à la résistance à la polymyxine pendant le stress de famine. Comparées à la souche de type sauvage (WT), les mutants Δppk présentent des défauts de croissance significatifs lorsqu’ils sont transférés dans un milieu minimal MOPS, tandis que les cellules WT présentent des défauts de croissance minimes dans cette condition carente en nutriments. Ce phénotype différentiel sert de lecture utile pour évaluer les inhibiteurs PPK. La délétion du transporteur de phosphate à faible affinité PitA sauve le défaut de croissance des mutants Δppk ; Cette interaction fait toujours l’objet d’une enquête. Différents médicaments réutilisés agissent comme inhibiteurs de la PPK, notamment la mésalamine (largement utilisée pour traiter les maladies inflammatoires de l’intestin telles que la maladie de Crohn et la colite ulcéreuse) et la galléine (à l’origine un colorant histologique et un inhibiteur de Gβγ). Les deux composés inhibent les enzymes PPK bactériennes. Dans cette étude, nous avons évalué les effets de la mésalazine et de la gallée sur les phénotypes de croissance de quatre souches d’E. coli (WT, Δppk, ΔpitA, et le double mutant ΔppkΔpitA) dans des conditions de manque de nutriments (milieu minimal MOPS). Les deux inhibiteurs n’ont produit qu’une légère altération de la croissance non spécifique entre souches, et cet effet n’a pas été amélioré par des concentrations plus élevées de médicaments. Le traitement par galléine n’a montré aucun effet clair sur les niveaux de polyP, et les niveaux de polyP après un traitement à la mésalaline n’ont pas été évalués. Ces résultats préliminaires ont mis en lumière la nécessité d’optimiser la délivrance de médicaments ou de stratégies alternatives d’inhibition pour reproduire pleinement les phénotypes d’une déficience génétique en polyP.

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Publié-e

2026-06-17

Numéro

Vol. 5 No. 2 (2026)

Rubrique

Résumés d’initiation à la recherche en sciences au premier cycle

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