CONICET | Buscador de Institutos y Recursos Humanos

Staphylococcus aureus is the causative agent of a broad spectrum of infections due to its ability to attach to damaged epithelia and inanimate surfaces, and to adopt a biofilm lifestyle. Biofilm is involved in the development of device-related infections and chronic infections of diverse tissues. During the biofilm development, the polysaccharide intercellular adhesin encoded by the icaADBC operon contributes to the bacterial agglomeration. The extracellular DNA from autolytic cells and several proteins are also involved in sticking the bacterial cells together. Unlike methicillin-resistant S. aureus (MRSA), available evidence indicates that biofilm formation by methicillin-susceptible S. aureus (MSSA) isolates depends upon the product of the icaADBC genes. The environmental conditions and metabolic status of the bacteria affect the biofilm formation. Salicylic acid (SAL), the main aspirin metabolite producted in vivo, interferes with expression of several S. aureus virulence factors (such as capsular polysaccharide, Eap) and global regulators (such as mgrA, saeRS). The aim of the present study was to investigate the effect of SAL on biofilm formation by S. aureus. Here, we demonstrate that SAL enhances biofilm production by both MSSA and MRSA strains. The principal component analyses in the polysaccharide external region (1200-800 cm-1 spectral range) from the Fourier-transform infrared spectroscopy data determined that SAL caused polysaccharide perturbations in S.aureus biofilm. Dispersal of established biofilm by enzymatic treatments was quantified to determine the contribution of proteins, extracellular DNA and polysaccharide into biofilm extracellular matrices induced by SAL. Taken together the results suggest that SAL promotes the biofilm formation by S. aureus which would contribute to the persistence of infection.