ArticleScientific reports2024
Filling knowledge gaps related to AmpC-dependent β-lactam resistance in Enterobacter cloacae.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Non canonical perspectives on AmpR mediated ampC expression in Gram negative bacteria, with particular emphasis on the potential regulatory purview of FtsZ.World journal of microbiology & biotechnology · 2026Review
- Evaluation of Three Treatments for the Resource Utilization of Cephalosporin C Fermentation Residue.Toxics · 2026Article
- Novel continuous experimental evolution methodology uncovers rapid resistance development and cross-resistance.npj antimicrobials and resistance · 2026Article
- Genomic analysis ofMicrobial genomics · 2026Article
- Molecular and pharmacodynamic insights into β-lactam therapy for high-inoculumAntimicrobial agents and chemotherapy · 2025Article
- Correlation between the mutation rates for ampC derepression and species or ampC genotypes in Enterobacter cloacae complex.BMC microbiology · 2025Article
- Distinct molecular epidemiology of resistances to extended-spectrum cephalosporins and carbapenems in Enterobacter hormaechei in cats and dogs versus horses in France.The Journal of antimicrobial chemotherapy · 2025Article
- Bacterial peptidoglycan as a living polymer.Current opinion in chemical biology · 2025Review
- Exploring nagZ as a virulence biomarker and treatment target in Enterobacter cloacae.BMC microbiology · 2025Article
- Cryo-EM characterization of the anydromuropeptide permease AmpG central to bacterial fitness and β-lactam antibiotic resistance.Nature communications · 2024Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Enterobacter cloacae starred different pioneer studies that enabled the development of a widely accepted model for the peptidoglycan metabolism-linked regulation of intrinsic class C cephalosporinases, highly conserved in different Gram-negatives. However, some mechanistic and fitness/virulence-related aspects of E. cloacae choromosomal AmpC-dependent resistance are not completely understood. The present study including knockout mutants, β-lactamase cloning, gene expression analysis, characterization of resistance phenotypes, and the Galleria mellonella infection model fills these gaps demonstrating that: (i) AmpC enzyme does not show any collateral activity impacting fitness/virulence; (ii) AmpC hyperproduction mediated by ampD inactivation does not entail any biological cost; (iii) alteration of peptidoglycan recycling alone or combined with AmpC hyperproduction causes no attenuation of E. cloacae virulence in contrast to other species; (iv) derepression of E. cloacae AmpC does not follow a stepwise dynamics linked to the sequential inactivation of AmpD amidase homologues as happens in Pseudomonas aeruginosa; (v) the enigmatic additional putative AmpC-type β-lactamase generally present in E. cloacae does not contribute to the classical cephalosporinase hyperproduction-based resistance, having a negligible impact on phenotypes even when hyperproduced from multicopy vector. This study reveals interesting particularities in the chromosomal AmpC-related behavior of E. cloacae that complete the knowledge on this top resistance mechanism.
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