Effect of salicylic acid on biofilm formation by Staphylococcus aureus strains

DOTTO C; GRUNERT T; CATTELÁN N; LOMBARTE A; SULIGOY C; YANTORNO O; SORDELLI D; BUZZOLA F

Córdoba

Congreso; XI Congreso Argentino de Microbiología General; 2015

Sociedad Civil de Microbiología General (SAMIGE)

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 (PIA) encoded by the icaADBC operon contributes to the bacterial agglomeration. The extracellular DNA (eDNA) 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 PIA production. The environmental conditions and metabolic status of the bacteria affect the biofilm formation. Salicylic acid (SAL), the main aspirin metabolite produced 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 and determine the nature of the biofilm?s matrices after the treatment with SAL. Biofilms formed by S. aureus were stained with crystal violet for spectrophotometric quantification. Detachment of preformed biofilms was determined after treating the biofilms with Dispersin B, proteinase K or DNAse I. Biofilms grown with or without SAL were analysed by Fourier transform infrared spectroscopy (FTIR) in the spectral range of 1,200 to 800 cm-1 (polysaccharides region). Here, we demonstrated that SAL enhances biofilm production in all strains under study. The principal component analyses in the polysaccharide external region from the FTIR data determined that SAL caused polysaccharide perturbations in S. aureus biofilms. Dispersal of stablished biofilm by enzymatic treatments shown that the extracellular matrices of the SAL treated-biofilms are mainly of proteinaceous and polysaccharide nature. The contribution of the eDNA would be not relevant. Taken together the results suggest that SAL promotes the biofilm formation by S. aureus which would contribute to the persistence of infection.