E. coli-synthesized selenium nanoparticles suppress phoP and bapA gene expression in S. enterica isolated from human blood

Abstract

Introduction: Typhoid fever is caused by Salmonella enterica, which is a chronic health problem in endemic areas due to multidrug resistance and biofilm development. The stress adaptation and virulence regulatory gene phoP and the biofilm-associated gene bapA may represent molecular targets for anti-virulence interventions. In this study, S. Typhi isolates from blood samples were characterized for their antimicrobial sensitivity and biofilm formation, and the molecular impact of biosynthesized selenium nanoparticles (SeNPs) on phoP and bapA expression was assessed.

Methodology: Biochemical analyses and 16S rRNA polymerase chain reaction (PCR) were performed on 92 blood samples identified 35 S. Typhi isolates. Antimicrobial susceptibility was evaluated by standard protocols. Biofilm-formation capacity was determined. SeNPs were obtained from E. coli by biological synthesis according to ultraviolet–visible (UV-vis) spectroscopy, Fourier-transform infrared (FTIR) spectroscopy, and X-ray diffraction (XRD) analyses; at concentrations of 12.5–100 µg/mL. Differences in gene expression were quantified by quantitative reverse transcription real-time PCR.

Results: All the isolates were resistant to ampicillin and ceftriaxone; susceptible to meropenem, ertapenem, trimethoprim–sulfamethoxazole, chloramphenicol, and tetracycline; and had variable sensitivity to ciprofloxacin. The isolates induced strong (57.1%) and moderate (40%) biofilm formation. The production of phoP and bapA were significantly inhibited by SeNPs treatment in a concentration-dependent manner, with maximal inhibition at 100 µg/mL (p = 0.0001); and exhibited a significant positive correlation for both genes (R = 0.899).

Conclusions: Biosynthesized SeNPs effectively downregulate key virulence determinants in antibiotic-resistant S. Typhi, supporting their potential as adjunctive or alternative therapies capable of decelerating pathogenicity and biofilm-associated persistence.