<i>Enterococcus faecalis</i> induces H₂O₂-mediated epithelial cell death and enhances <i>Candida albicans</i> virulence in oropharyngeal candidiasis

Chemotherapy-induced mucosal barrier injury and immune suppression increase susceptibility to oropharyngeal candidiasis (OPC), a debilitating fungal infection. Our study uncovers a previously unknown pathogenic interaction between <i>Candida albicans</i> and <i>Enterococcus faecalis</i>, by showing that indigenous enterococci produce H₂O₂, which contributes to oral epithelial cell death during fungal infection. By integrating transcriptomics with functional assays, we demonstrate that enterococci compromise epithelial integrity independently of fungal burdens, highlighting the role of the bacterial microbiota in driving tissue damage. These findings emphasize the need to consider bacterial-fungal interactions in managing OPC and suggest that targeting the microbial crosstalk could be a promising adjunctive strategy in immunocompromised hosts.