Good news!
"... has discovered a new method that could speed up the healing of chronic wounds infected by antibiotic-resistant bacteria. ...
The team discovered that unlike other bacteria, which produce toxins when they infect wounds, E. faecalis produces a metabolic product called reactive oxygen species (ROS) that impairs the healing process of human skin cells. ...
E. faecalis uses a metabolic process known as extracellular electron transport (EET), which continuously produces hydrogen peroxide, a highly reactive oxygen species that can damage living tissue.
When present in infected wounds, this bacterium produces hydrogen peroxide, which damages human skin cells through oxidative stress.
Laboratory experiments showed that oxidative stress triggers a cellular defense mechanism known as the "unfolded protein response" in skin cells called keratinocytes, which are responsible for skin repair. This unfolded protein response is normally used by cells to cope with damage by slowing down protein production and other vital activities, so that they can recover. Once activated, the stress response effectively paralyzes the cells, preventing them from moving to close the wound, a process known as migration.
When the researchers used a genetically modified strain of E. faecalis that lacked the EET pathway, the bacteria produced significantly less hydrogen peroxide and were unable to block wound healing.
This confirmed that the metabolic pathway was central to the bacterium's ability to disrupt skin repair. The team then tested whether neutralizing the hydrogen peroxide could reverse the damage.
Potential solution that bypasses antibiotic-resistance
By treating affected skin cells with catalase, a naturally occurring antioxidant enzyme that breaks down hydrogen peroxide, the researchers reduced cellular stress and thus restored the cells' ability to migrate and heal."
From the abstract:
"Enterococcus faecalis is an opportunistic pathogen that thrives in biofilm-associated infections and delays wound healing, yet how it impairs host tissue responses is unclear.
Here, we identified extracellular electron transport (EET) as a previously unrecognized source of reactive oxygen species (ROS) in E. faecalis and showed that this activity directly triggers the unfolded protein response (UPR) in epithelial cells and delays epithelial cell migration.
ROS detoxification with catalase suppressed E. faecalis–induced UPR and rescued epithelial cell migration, while exogenous hydrogen peroxide was sufficient to restore UPR activation in EET-deficient strains.
UPR disruption by pharmacological inhibition also impaired cell migration, highlighting a critical role for UPR homeostasis in wound repair.
Our findings establish EET as a virulence mechanism that links bacterial redox metabolism to host cell stress and impaired repair, offering previously unidentified avenues for therapeutic intervention in chronic infections."
Enterococcus faecalis redox metabolism activates the unfolded protein response to impair wound healing (open access)
Fig. 1. E. faecalis infection activates the UPR in a mouse model.
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