Background
Enterococci have emerged as a global cause of nosocomial infection and are frequently associated with chronic ulcers, urinary tract infections, endocarditis and indwelling medical device-related infections. The robust biofilm formation and inherent multidrug resistance in Enterococci have uplifted it as a challenging nosocomial pathogen. Biofilms are cell populations irreversibly attached to surfaces and encased within a self-produced hydrated matrix of exopolymeric substances, proteins, polysaccharides, extracellular DNA (eDNA) and water channels. Biofilm confers high antibiotic tolerance ability and resistance to phagocytosis and hence play a prime role in critical colonization, establishment and chronicity of infections. This renders Enterococci to be recalcitrant towards the current treatment strategies. Owing to its egressing clinical significance, the pace of enterococcal biofilm research has accelerated in the past few years for providing a better understanding of intricate underlying mechanisms of biofilm formation.
In E.faecalis, fsr two-component signal transduction system is a well-defined quorum sensing system which regulates biofilm formation by gelatinase production [1]. Previous studies on enterococcal biofilm have suggested several other biofilm associated factors including enterococcal surface protein (esp) [2], aggregation substance [3], pili [4], autolysin [5] and D-alanylation of Lipoteichoic acid (dltABCD) [6]. Several studies on E. faecalis comparing biofilm formers and non-biofilm formers have identified protein translation machinery, aromatic amino acid biosynthesis and sugar and sulfate permease transporter systems to have a momentous role in biofilm formation [7, 8]. E. faecalis SK460 used in the present study is isolated from a chronic diabetic ulcer patient [9] and is devoid of several well-defined biofilm associated factors including fsr quorum signaling, gelatinase production and enterococcal surface protein. Lack of these biofilm determinants does not affect the biofilm forming potential of SK460. This led us to focus on the role of differential protein expression pattern in biofilm phenotype of this strong biofilm former. The present study utilized label-free quantitative approach to decipher the protein expression pattern of E. faecalis SK460 at planktonic and biofilm stages to elucidate the unexplored links in understanding the enterococcal biofilms. This helps to deliver the comprehensive knowledge regarding the metabolic pathways and cellular processes involved in Enterococcal biofilm to come up with potential biofilm inhibiting targets.