Staphylococcus aureus Pathogenesis Within the Polymicrobial Diabetic Wound

Diabetes is a chronic condition and a pervasive health crisis around the world. One of the major complications of diabetes is the development of foot ulcers due to neuropathy or poor circulation combined with sustained hyperglycemia. These foot ulcerations often become chronic wounds that are slow to heal and susceptible to infection. Moreover, many diabetic foot infections are polymicrobial, with Staphylococcus aureus being the most common causative organism. We previously established a diabetic wound polymicrobial infection model in SKH1-Elite hairless mice and observed that S. aureus exhibits decreased dissemination from the wound and decreased expression of virulence genes when in co-infection with Enterococcus faecalis, another common microbe in diabetic foot infections. However, previous work has not yet elucidated the mechanism of action which leads to the observed commensalism. Here, we aimed to investigate the identity and mechanism of the secreted E. faecalis factor that promotes S. aureus commensalism through isolating E. faecalissupernatant components and observing subsequent effects on S. aureus hemolytic activity. Our results suggest a small, heat-resistant polysaccharide or peptide which may interact with S. aureus hemolysins. These findings may offer novel information on S. aureus pathogenesis in the diabetic wound and improve strategies for treatment of infection.