A team of 12 researchers from University Hospital of Geneva, Switzerland and the Institute of Food Research, Norwich, UK set out to uncover what S. aureus (6850) did inside human lung epithelial cells (A549) using an in vitro model.
They found that shortly after S. aureus entered the lung cells, the bacteria’s gene expression profile dramatically changed: gene expression for bacterial metabolic functions and transport shut down, putting the bacteria in a dormant state. Simultaneously, production of toxins potentially lethal for the epithelial cells becomes strictly controlled to limit cellular damage.
Mechanisms that helped the bacteria to survive and/or multiply, including metabolic and energy production functions, then resumed. Although most of the bacteria had died by about four days as a result of antibiotic treatment, the team still found viable bacteria in their model system two weeks after infection.
The findings may help in understanding persistent infections, and in designing new antibacterial drugs. S. aureus has not traditionally been considered an intracellular pathogen, but the molecular details that govern its extended persistence remain largely unknown. The bacteria can generate relapsing infections even years after the first episode was apparently cured.
“S. aureus intracellular survival appears related to its capability to adopt a discrete behaviour instead of actively duplicating,” says Patrice Francois, a Geneva-based member of the research team. “S. aureus then benefits from natural or programmed cell death to re-emerge and trigger another episode of infection, leading to chronicity.”
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