SORDELLI Daniel Oscar
congresos y reuniones científicas
Biofilm formation by Staphylococcus aureus strains exposed to salicylic acid.
DOTTO C; GRUNERT T; CATTELAN N; LOMBARTE SERRAT A; YANTORNO O; EHLING-SCHULTZ M; SORDELLI DO; BUZZOLA FR
CHICAGO, ILLINOIS, USA
Simposio; International Symposium on Staphylococcus and Staphylococcal Infections (ISSSI); 2014
International Symposium on Staphylococcus and Staphylococcal Infections (ISSSI)
Staphylococcus aureus is the causative agent ofa broad spectrum of infections due to its ability to attach to damagedepithelia and inanimate surfaces, and to adopt a biofilm lifestyle. Biofilm isinvolved in the development of device-related infections and chronic infectionsof diverse tissues. During the biofilm development, the polysaccharideintercellular adhesin encoded by the icaADBC operon contributes to the bacterialagglomeration. The extracellular DNA from autolytic cells and several proteinsare also involved in sticking the bacterial cells together. Unlikemethicillin-resistant S. aureus (MRSA), available evidence indicates that biofilmformation by methicillin-susceptible S. aureus (MSSA) isolates depends upon the product ofthe icaADBC genes. The environmentalconditions and metabolic status of the bacteria affect the biofilm formation.Salicylic acid (SAL), the main aspirin metabolite producted in vivo, interferes withexpression of several S. aureus virulence factors (such as capsularpolysaccharide, Eap) and global regulators (such as mgrA, saeRS). The aim of the present study was to investigate theeffect of SAL on biofilm formation by S. aureus. Here, we demonstrate that SAL enhancesbiofilm production by both MSSA and MRSA strains. The principal componentanalyses in the polysaccharide external region (1200-800 cm-1 spectral range)from the Fourier-transform infrared spectroscopy data determined that SALcaused polysaccharide perturbations in S. aureus biofilm. Dispersal of established biofilm byenzymatic treatments was quantified to determine the contribution of proteins,extracellular DNA and polysaccharide into biofilm extracellular matricesinduced by SAL. Taken together the results suggest that SAL promotes thebiofilm formation by S. aureus which would contribute to the persistence ofinfection.