Bio-engineered silver nanoparticles suppress flic-mediated motility and induce argI-driven metabolic rewiring in Escherichia coli

Abstract

The rise of antimicrobial resistance necessitates novel treatment approaches, with bio-synthesized nanoparticles offering promising alternatives. This study explores silver nanoparticles (bio-AgNPs) synthesized using Terminalia chebula extract, characterized via spectroscopy and microscopy techniques. Bio-AgNPs exhibited a surface plasmon resonance peak at 466 nm, an average hydrodynamic diameter of 150.3 nm, and a zeta potential of −41.55 mV, ensuring colloidal stability. Antibacterial efficacy was evaluated against Escherichia coli K12, with a minimum inhibitory concentration of 78.125 ppm. Transcriptomic profiling revealed a significant downregulation of flagellar biosynthesis and assembly genes—including fliC (encoding flagellin, the main structural protein of bacterial flagella), flgB, flgC, flgD, flgE, fliH, flgG, fliI, flgH, fliJ, and fliK—impairing bacterial chemotaxis and reducing motility. Concurrently, suppression of the citT gene disrupted citrate import via the citrate-succinate antiporter, impairing TCA cycle flux and limiting carbon metabolism. Conversely, genes involved in L-arginine biosynthesis and transport—including argI (encoding ornithine carbamoyltransferase, a key enzyme in the arginine biosynthesis pathway), argC, carA, argD, argA, argG, artP, artQ, artJ, and artI—were upregulated, indicating a metabolic shift toward arginine catabolism via the arginine deiminase pathway under oxidative stress. Arginine is known to inhibit Na⁺-Na-dependent flagellar motors by competitively interfering with sodium binding, further exacerbating motility impairment. The dual antimicrobial action—disrupting flagellar function and inducing metabolic stress—suggests a potent biochemical mechanism to counteract bacterial adaptation and resistance.