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Multidrug-resistant threatens both sustainable aquaculture and human health, but the control measure is still lacking. In this study, we adopted functional proteomics to investigate the molecular mechanism underlying norfloxacin (NOR) resistance in . We found that had a global proteomic shift upon acquisition of NOR resistance, featured with increased expression of siderophore biosynthesis and Fe-hydroxamate transport. Thus, either inhibition of siderophore biosynthesis with salicyl-AMS or treatment with another antibiotic, kitasamycin (Kit), which was uptake through Fe-hydroxamate transport, enhanced NOR killing of NOR-resistant both and . Moreover, the combination of NOR, salicyl-AMS, and Kit had the highest efficacy in promoting the killing effects of NOR than any drug alone. Such synergistic effect not only confirmed and bacterial killing assays but also applicable to other clinic isolates. Thus, our data suggest a proteomic-based approach to identify potential targets to enhance antibiotic killing and propose an alternative way to control infection of multidrug-resistant .
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http://dx.doi.org/10.1021/acs.jproteome.3c00365 | DOI Listing |
Plant Physiol
September 2025
Plant Physiology, American Society of Plant Biologists.
Vestn Oftalmol
September 2025
Helmholtz National Medical Research Center of Eye Diseases, Moscow, Russia.
The etiology of uveitis, choroid inflammation, is diverse, the disease is often recurrent, difficult to treat, and frequently results in disability at a young age. Studies investigating the tear fluid composition in uveitis have revealed promising biomarkers relevant for prognosis and treatment optimization. This review presents literature data on changes in the tear fluid content of proteins involved in local immune responses, intercellular interactions, proteolytic and free radical processes, nitric oxide metabolism, and other metabolic pathways in different forms of uveitis.
View Article and Find Full Text PDFJ Invest Dermatol
September 2025
Department of Dermatology, Keck School of Medicine of University of South California, Los Angeles, California, USA; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan. Electronic address:
This review examines the roles of galectins, a family of animal lectins, in inflammatory skin diseases, focusing on their involvement in the pathogenesis of psoriasis, atopic dermatitis, contact dermatitis, and common autoimmune diseases. We highlight the differential expression of galectins in lesional skin and their correlation with inflammatory mediators. In addition, we summarize the functions and mechanisms of action of endogenous galectins, as revealed through studies of genetically engineered cell lines and experimental animals.
View Article and Find Full Text PDFmSphere
September 2025
Leiden Institute of Chemistry and The Institute of Chemical Immunology, Leiden University, Leiden, the Netherlands.
Bacterial persisters are a subpopulation of cells that exhibit a transient non-susceptible phenotype in the presence of bactericidal antibiotic concentrations. This phenotype can lead to the survival and regrowth of bacteria after treatment, resulting in relapse of infections. It is also a contributing factor to antibacterial resistance.
View Article and Find Full Text PDFBrain
September 2025
Central European Institute of Technology Masaryk University (CEITEC MU), 625 00 Brno, Czech Republic.
Mutations in the human ADAR gene encoding adenosine deaminase acting on RNA 1 (ADAR1) cause Aicardi-Goutières syndrome 6 (AGS6); a severe auto-inflammatory encephalopathy with aberrant interferon (IFN) induction. AdarΔ2-13 null mutant mouse embryos lacking ADAR1 protein die with high levels of IFN-stimulated gene (ISG) transcripts. In Adar Mavs double mutants also lacking the Mitochondrial antiviral signaling (MAVS) adaptor, the aberrant IFN induction is prevented.
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