Singapore study links common bacterium to slow-healing wounds
Photo: SMART AMR
Researchers from the Singapore-MIT Alliance for Research and Technology (SMART) and partner institutions have identified how a common bacterium disrupts the body’s immune response, contributing to persistent and hard-to-treat wound infections.
The study focused on Enterococcus faecalis, a bacterium frequently found in chronic wounds. According to the research team, the microbe releases large amounts of lactic acid, which lowers the pH of its surroundings and interferes with immune signaling. This process prevents immune cells from mounting an effective response, allowing infections to persist.
As described in the study published in Cell Host & Microbe, the acidic environment suppresses the activation of macrophages, which are key immune cells responsible for detecting and clearing infections. The lactic acid disrupts internal signaling pathways, including the NF-κB pathway, which is essential for triggering immune defenses.
The researchers explained that the bacterium uses a two-step mechanism. Lactic acid enters immune cells through a transporter known as MCT-1 and also binds to a receptor called GPR81 on the cell surface. By acting on both pathways, the bacterium effectively shuts down immune signaling and reduces inflammation, enabling it to survive longer in the wound.
Findings from a mouse model showed that strains of E. faecalis unable to produce lactic acid were cleared more quickly and triggered stronger immune responses. The study also found that in mixed infections, the weakened immune environment allowed other bacteria such as Escherichia coli to grow more easily, which helps explain why chronic wounds often involve multiple bacterial species.
According to Dr Ronni da Silva, the study suggests that chronic wound infections persist not only because of antibiotic resistance but also because the immune system is suppressed at the infection site. He said that the buildup of lactic acid effectively silences key immune signals, preventing macrophages from responding properly.
Professor Kimberly Kline added that the findings improve understanding of how bacteria interact with the host immune system and may inform new treatment strategies. She said targeting the bacterium’s ability to suppress immune responses could support better infection management and recovery outcomes.
The researchers said the findings point to new approaches that go beyond antibiotics, including therapies that reduce acidity in wounds or block the pathways used by lactic acid to inhibit immune cells. Future work will focus on validating the results in human samples and advancing toward preclinical studies.
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