Researchers from SMART and collaborators have uncovered how Enterococcus faecalis bacteria evade immune defenses in chronic wound infections. The bacterium releases large amounts of lactic acid, which acidifies the wound environment and suppresses macrophage activation through two pathways: entering cells via the MCT-1 lactate transporter and binding to the GPR81 receptor on the cell surface. Both pathways block the NF-κB immune signaling cascade, preventing macrophages from mounting a proper inflammatory response. This immune suppression also enables other bacteria like E. coli to thrive, explaining why polymicrobial wound infections are so difficult to treat. Mouse model experiments confirmed that E. faecalis strains unable to produce lactic acid were cleared faster and triggered stronger immune activity. The findings point toward new treatment strategies targeting wound acidity or lactic acid signaling pathways to reactivate immune responses, potentially reducing reliance on antibiotics alone.
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