Bacteria Suppress Immune Defenses in Wound Infections
Summary: Researchers from the Singapore-MIT Alliance for Research and Technology (SMART) AMR group discovered that Enterococcus faecalis, a common bacterium in chronic wounds, releases lactic acid to suppress macrophage activation and immune response. Lactic acid enters macrophages through the MCT-1 transporter and binds the GPR81 receptor, blocking downstream NF-κB signaling and preventing effective inflammation and bacterial clearance. In mouse wound models, lactic acid-deficient E. faecalis strains were cleared faster with stronger immune activity. The mechanism also facilitates co-infection with other bacteria like E. coli, explaining why polymicrobial infections in diabetic foot ulcers and other chronic wounds are persistent and difficult to treat. The findings suggest new therapeutic strategies focused on neutralizing acidity or restoring immune function rather than antibiotics alone.
Key Highlights:
- E. faecalis lactic acid inhibits macrophage activation via MCT-1 and GPR81
- Blocks NF-κB signaling, allowing persistent and polymicrobial wound infections
- Stronger immune clearance when lactic acid production is absent in mouse models
- Implications for chronic wounds including DFU and post-surgical infections
Keywords: Enterococcus faecalis, lactic acid wounds, macrophage suppression, polymicrobial infections