Chronic wounds, like diabetic foot ulcers, are a growing problem around the world. They often last for months or even years, putting people at risk of serious complications, including amputations.
Each year, over 18 million people develop diabetic foot ulcers globally, and up to one in three people with diabetes may experience one at some point in their life. In Singapore alone, more than 16,000 chronic wound cases are reported every year, mostly among older adults and people with diabetes.
Now, researchers from Nanyang Technological University (NTU Singapore), along with international collaborators, have found a promising new way to help these stubborn wounds heal—without relying on antibiotics.
The study, published in Science Advances, focuses on a common bacterium called Enterococcus faecalis (E. faecalis), which is often found in wounds that won’t heal.
These types of wounds are not only hard to treat, but many of the bacteria inside them are becoming resistant to antibiotics. This makes infections even harder to control. Scientists have known for a long time that infections slow down healing, but they didn’t fully understand why.
This study offers a new explanation. Instead of releasing harmful toxins like many bacteria do, E. faecalis uses a different strategy.
It produces a chemical called hydrogen peroxide through a process in its metabolism called extracellular electron transport (EET). Hydrogen peroxide is a reactive oxygen species (ROS) that can damage cells by causing a type of stress known as oxidative stress.
In experiments, the researchers found that hydrogen peroxide from E. faecalis affects nearby human skin cells, especially keratinocytes—the cells that help repair skin.
These cells respond by activating a stress reaction called the “unfolded protein response.” Normally, this helps protect the cell, but in this case, it ends up freezing the cell’s ability to move and repair the wound.
The research team confirmed this by creating a version of E. faecalis that lacked the EET pathway. These bacteria produced less hydrogen peroxide and were no longer able to stop the skin cells from healing the wound. This proved that the bacteria’s metabolism, not just its presence, plays a major role in preventing wounds from healing.
To counteract this harmful effect, the scientists used an antioxidant enzyme called catalase. Catalase naturally breaks down hydrogen peroxide into harmless water and oxygen. When skin cells exposed to E. faecalis were treated with catalase, they began healing again. The cells were able to move and cover the wound, just like healthy skin should.
This approach is especially exciting because it does not depend on antibiotics. Instead of killing the bacteria, it neutralizes the harmful substances the bacteria produce. This method could avoid the problem of antibiotic resistance, which is becoming more and more serious worldwide.
Associate Professor Guillaume Thibault, one of the study’s leaders, explained, “Our findings show that the bacteria’s metabolism is the real problem. By neutralizing its byproducts instead of trying to kill the bacteria, we can promote healing without contributing to the rise of antibiotic resistance.”
The team believes their discovery could lead to new treatments for chronic wounds. For example, future wound dressings could be infused with antioxidants like catalase. Since catalase is already well known and widely used, it may be faster to turn this idea into a real treatment, compared to developing a brand-new drug.
Because the study used human skin cells, the results are very relevant to real-world medicine. The next step is to test the treatment in animals and then move to human clinical trials.
This research provides hope for millions of people who suffer from wounds that refuse to heal. By targeting the effects of bacterial metabolism instead of the bacteria themselves, scientists may have found a safer, more effective way to support the body’s natural healing process.
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