Unweaving the role of staphylococcal enterotoxins in the pathogenesis of infective endocarditis

Staphylococcus aureus is a bacterium that causes a variety of infections from minor skin and soft tissue infections to more invasive infections of the heart and lungs. S. aureus uses a number of toxins to cause infection. Superantigens are a group of S. aureus toxins that disrupt proper function of the immune system. The superantigens, SEC and the egc, were previously shown to be critical for S. aureus to cause a heart infection called infective endocarditis. Although the importance of these superantigens has been established, the mechanism behind their importance is not known. Recently, superantigens have been shown to have alternate functions that differ from their established function of immune system disruption. We sought to determine if disruption of the immune system or an uncharacterized alternate function was responsible for the importance of SEC in S. aureus infective endocarditis. Our findings indicate that SEC promotes S. aureus infective endocarditis through a new mechanism by interacting with the heart tissue. The CC5 S. aureus lineage is a highly prevalent group in S. aureus infection. Although it has high prevalence, the CC5 lineage has not been well characterized. Here we established the CC5 lineage as a model group to study the importance of the egc in infective endocarditis. Taken together, our findings establish a new mechanistic basis for superantigens involvement in S. aureus infective endocarditis and opens the door for new mechanistic studies of the egc in the CC5 S. aureus clonal lineage.