BibTex format
@article{Kadeřábková:2025:10.1101/2023.08.02.551661,
author = {Kadeábková, N and Furniss, RCD and Maslova, E and Potter, KE and Eisaiankhongi, L and Bernal, P and Filloux, A and Landeta, C and Gonzalez, D and McCarthy, RR and Mavridou, DAI},
doi = {10.1101/2023.08.02.551661},
journal = {bioRxiv},
title = {Antibiotic potentiation and inhibition of cross-resistance in pathogens associated with cystic fibrosis.},
url = {http://dx.doi.org/10.1101/2023.08.02.551661},
year = {2025}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Critical Gram-negative pathogens, like Pseudomonas, Stenotrophomonas and Burkholderia, have become resistant to most antibiotics. Complex resistance profiles together with synergistic interactions between these organisms increase the likelihood of treatment failure in distinct infection settings, for example in the lungs of cystic fibrosis (CF) patients. Here, we discover that cell envelope protein homeostasis pathways underpin both antibiotic resistance and cross-protection in CF-associated bacteria. We find that inhibition of oxidative protein folding inactivates multiple species-specific resistance proteins. Using this strategy, we sensitize multidrug-resistant Pseudomonas aeruginosa to β-lactam antibiotics and demonstrate promise of new treatment avenues for the recalcitrant emerging pathogen Stenotrophomonas maltophilia. The same approach also inhibits cross-protection between resistant S. maltophilia and susceptible P. aeruginosa, allowing eradication of both commonly co-occurring CF-associated organisms. Our results provide the basis for the development of next-generation strategies that target antibiotic resistance, while also impairing specific interbacterial interactions that enhance the severity of polymicrobial infections.
AU - Kadeábková,N
AU - Furniss,RCD
AU - Maslova,E
AU - Potter,KE
AU - Eisaiankhongi,L
AU - Bernal,P
AU - Filloux,A
AU - Landeta,C
AU - Gonzalez,D
AU - McCarthy,RR
AU - Mavridou,DAI
DO - 10.1101/2023.08.02.551661
PY - 2025///
TI - Antibiotic potentiation and inhibition of cross-resistance in pathogens associated with cystic fibrosis.
T2 - bioRxiv
UR - http://dx.doi.org/10.1101/2023.08.02.551661
UR - https://www.ncbi.nlm.nih.gov/pubmed/37577508
ER -