RESUMEN
Urinary tract infections (UTIs) are a major public health concern in both community and hospital settings worldwide. Uropathogenic Escherichia coli (UPEC) is the main causative agent of UTI and increasingly associated with antibiotic resistance. Herein, we report the draft genome sequence of 9 fluoroquinolone-resistant UPEC isolates from Brazil and examine selected major phenotypic features, such as antimicrobial resistance profile, phylogroup, serotype, sequence type (ST), virulence genes, and resistance marks. Besides the quinolone resistance, beta-lactams, ESBL production, aminoglycosides, and tetracycline resistance were observed. High prevalence of 20 virulence genes was detected in all isolates, such as those encoding type 1 fimbriae, acid tolerance system, and hemolysin E, particularly within E. coli B2 phylogroup, as ST131 and ST1193 strains, among other genomic analyses as genomic islands, resistance plasmids, and integron identification.
Asunto(s)
Infecciones por Escherichia coli , Genoma Bacteriano , Infecciones Urinarias , Escherichia coli Uropatógena , Brasil , Farmacorresistencia Bacteriana , Infecciones por Escherichia coli/microbiología , Fluoroquinolonas/farmacología , Humanos , Infecciones Urinarias/microbiología , Escherichia coli Uropatógena/efectos de los fármacos , Escherichia coli Uropatógena/genética , Factores de Virulencia/genéticaRESUMEN
The aims of this work were to evaluate the antibacterial and antiproliferative potential in vitro of the metal complex with 4-aminobenzoic acid (Ag-pABA) and a drug delivery system based on bacterial cellulose (BC-Ag-pABA). The Ag-pABA complex was characterized by elemental analysis, high resolution mass spectrometry and single-crystal X-ray diffraction techniques, which indicated a 1:2 metal/pABA composition plus a nitrate ion coordinated to silver by the oxygen atom, with the coordination formula [Ag (C7H7NO2)2(NO3)]. The coordination of pABA to the silver ion occurred by the nitrogen atom. The in vitro antibacterial activity of the complex evaluated by minimum inhibitory concentration assays demonstrated the effective growth inhibitory activity against Gram-positive, Gram-negative biofilm producers and acid-alcohol resistant Bacillus. The antiproliferative activities against a panel of eight tumor cells demonstrated the activity of the complex with a significant selectivity index (SI). The DNA interaction capacity and the Ames Test indicated the absence of mutagenicity. The BC-Ag-pABA composite showed an effective capacity of sustained release of Ag-pABA. The observed results validate further studies on its mechanisms of action and the conditions that mediate the in vivo biological effects using animal models to confirm its safety and effectiveness for treatment of skin and soft tissues infected by bacterial pathogens, urinary tract infections and cancer.
Asunto(s)
Ácido 4-Aminobenzoico/química , Antibacterianos/farmacología , Bacterias/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Celulosa/química , Plata/farmacología , Antibacterianos/química , Preparaciones de Acción Retardada , Pruebas de Sensibilidad Microbiana , Plata/químicaRESUMEN
Intestinal bacteria employ microbial metabolites from the microbiota and chemical signaling during cell-to-cell communication to regulate several cellular functions. Pathogenic bacteria are extremely efficient in orchestrating their response to these signals through complex signaling transduction systems. Precise coordination and interpretation of these multiple chemical cues is important within the gastrointestinal (GI) tract. Enteric foodborne pathogens, such as enterohemorrhagic Escherichia coli (EHEC) and Salmonella enterica serovar Typhimurium, or the surrogate murine infection model for EHEC, Citrobacter rodentium, are all examples of microorganisms that modulate the expression of their virulence repertoire in response to signals from the microbiota or the host, such as autoinducer-3 (AI-3), epinephrine (Epi), and norepinephrine (NE). The QseBC and QseEF two-component systems, shared by these pathogens, are involved in sensing these signals. We review how these signaling systems sense and relay these signals to drive bacterial gene expression; specifically, to modulate virulence. We also review how bacteria chat via chemical signals integrated with metabolite recognition and utilization to promote successful associations among enteric pathogens, the microbiota, and the host.