Copper (Cu) plays a key role at the host-pathogen interface as both an essential element and a toxic element. Intracellular strains of pathogenic Salmonella have acquired the periplasmic Cu chaperone, CueP, and the thiol oxidoreductases complex Scs, while losing the ancestral Cu-detoxification Cus system. Coregulation of these species-specific factors link Cu with redox stress and allows Salmonella to counteract Cu toxicity during infection.
Keywords: CueP and Cus; bacterial envelope; copper; enteropathogens; host–pathogen interaction.
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