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Both per- and polyfluoroalkyl substances (PFASs) pollution and antibiotic resistance genes (ARGs) dissemination pose significant threats to global public health. PFASs and ARGs coexist in the environment, but little research was done on associations between PFASs and ARGs dissemination. This study demonstrated that perfluorooctane sulfonate (PFOS) increased ARGs transformation by 1.5-1.7-fold in Escherichia coli DH5α carrying pBR322 plasmid as a model. Moreover, pre-exposure of DH5α to PFOS increased ARGs transformation up to 7-fold. PFOS triggered up-regulation of the gene of outer membrane protein A (OmpA), enhancing cell membrane permeability and thus increasing ARGs transformation. Interestingly, the presence of ARGs decreased ompA gene expression and consequently lowered the accumulation and toxicity response of transformants to PFOS, which established cross-resistance between antibiotics and PFOS. This cross-resistance is attributed to the multifunctional role of the OmpA that acted as a major channel for ARGs entry into cells and facilitated cellular accumulation of PFOS. The OmpA-mediated cellular accumulation was also observed in structurally analogous PFASs (perfluorohexylsulfonic acid and pentadecafluorooctanoic acid), indicating a potential universality in the cross-resistance between antibiotics and PFASs. The United States, Canada and China are likely being confronted with high risks of PFOS-induced ARGs dissemination based on the global risk assessments. These findings demonstrate the overlooked eco-environmental risks associated with the interactions among PFASs, ARGs, and microorganisms, highlighting adaptability of organisms to chemical stress.
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http://dx.doi.org/10.1016/j.watres.2025.123868 | DOI Listing |
Antibiotics (Basel)
August 2025
Facultad de Ciencias Químicas, Universidad Autónoma de Nuevo León (UANL), San Nicolás de los Garza 66455, Mexico.
Antimicrobial resistance (AMR) poses a significant global health threat, necessitating a deeper understanding of bacterial adaptation mechanisms. This study investigates the genotypic and phenotypic evolutionary trajectories of under meropenem and gentamicin selection, and it benchmarks these findings against florfenicol-evolved strains. Utilizing a downsized, three-layer acrylic modified "Microbial Evolution and Growth Arena (MEGA-plate) system"-scaled to 40 × 50 cm for sterile handling and uniform 37 °C incubation-we tracked adaptation over 9-13 days, enabling real-time visualization of movement across antibiotic gradients.
View Article and Find Full Text PDFmSphere
August 2025
Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
To combat the growing threat of multidrug-resistant bacteria, we need to develop novel antibiotics with unique modes of action. This study investigates the antibacterial properties of BTP-001 toward . BTP-001 targets the β-clamp subunit of the DNA Pol III holoenzyme and is composed of the binding motif APIM linked to a cell-penetrating part composed of 11 arginine residues (R11).
View Article and Find Full Text PDFSci Rep
August 2025
IAME, UMR 1137, INSERM, Université Paris Cité, Paris, France.
Klebsiella pneumoniae carbapenemase (KPC) is a frequent and widespread carbapenemase, with over 260 variants identified. While KPC often evolves resistance to ceftazidime-avibactam, cefiderocol remains a key treatment option. Some variants, such as KPC-33 (D179Y), reduce cefiderocol susceptibility, but typically with only modest MIC increases.
View Article and Find Full Text PDFCurr Microbiol
August 2025
Institute of Pharmacy, Guangxi University of Chinese Medicine, Guangxi, 530001, People's Republic of China.
This study aimed to investigate the underlying mechanism of action and further identify main active ingredient by which Radix Paeoniae Rubra extracts (RPRE) inhibited the cross-resistance to tetracycline (TET), piperacillin (PIP), and gentamicin (GEN) mediated by Rhizoma Coptidis extracts (RCE) in Staphylococcus aureus (SA). Treatment with mixed solutions of RCE and RPRE resulted in disappearance of TET, PIP, or GEN resistance compared to what was shown with RCE treatment alone. Fifteen relevant resistant genes (smrB, bmr3, nhoA, BTN44_15030, clpL, hisG, norA, fmtA_1, emrB_1, BTN44_07590, paiA, icaR, BTN44_13995, HMPREF0776_1664 and vraG) were significantly downregulated compared to the RCE-induced mutants.
View Article and Find Full Text PDFNat Ecol Evol
August 2025
Department of Microbial and Molecular Systems, Centre of Microbial and Plant Genetics, KU Leuven, Leuven, Belgium.
With antibiotic resistance on the rise and the development of new antibiotics stagnating, novel antimicrobial strategies that slow down resistance evolution and extend the lifetime of existing drugs are urgently needed. One possible solution focuses on rationalizing antimicrobial combination and cycling therapies on the basis of the concept of collateral sensitivity, in which resistance mutations acquired against one antibiotic increase the susceptibility towards a second antibiotic. However, the clinical potential of collateral sensitivity is still uncertain as collateral responses for the same combination of antibiotics may vary from collateral sensitivity to cross-resistance, depending on stochasticity, environmental conditions and the genetic background of the pathogen.
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