We have previously shown that the replacement of DGlcDAG with MGlcDAG leads to a significantly impaired biofilm production in vitro and in vivo in a mouse sepsis model. On the other hand, cell morphology, autolysis, growth rate or expression of cell wall-associated proteins were not altered in these mutants. The role of glycolipids in vivo has already been assessed in mouse bacteremia models and a reduced persistence of bacteria in blood, liver, kidneys and spleens has been documented. However, these models do not represent typical biofilm infections. Certainly our results have to be interpreted cautiously. First of all the small sample size weakens the results with regard to statistical power, although our experience with this model of infective endocarditis taught us that results are reproducible. Furthermore the extent of non-infective thrombotic endocarditis plays a crucial role in the secondary bacterial colonization. To ensure constant non-infective lesions, we assessed the proper placement of the catheter and assessed the lesions themselves in preliminary tests. Since we did not measure blood stream survival of the inoculated bacteria, the influence of direct bloodstream clearance or the increased sensitivity of the mutants to the innate immune functions of the animals cannot be differentiated. Nevertheless previous data from our group show that the deletion of glucosyltransferase bgsB has no effect on resistance to complement, antimicrobial peptides, and opsonophagocytic killing. The bgsA deletion mutant showed higher susceptibility to opsonophagocytic killing, but comparable sensitivity to complement-mediated killing. Although the significantly reduced endocarditic lesions might be a direct effect of impaired biofilm accumulation on the heart valve itself our results cannot Danshensu clarify if the reduced virulence of the mutant strains is caused by interaction with host defense instead. In addition we could identify a putative virulence factor for enterococcal endocarditis, which might offer new therapeutic approaches. Guo et al. for example reported the use of antisense oligodeoxyribonucleotides as a way of gene silencing in Streptococcus mutants as a novel approach to decrease biofilm formation. Specific small molecule inhibitors of genes essential for virulence but not directly toxic for bacteria may exert less selective pressure to develop resistances and may be therefore a ractive novel therapeutic approaches. Our results indicate that the model presented here is suitable to assess specific virulence factors of enterococcal strains involved in biofilm infections. This will allow the detection and confirmation of additional virulence factors and may lead to the development of novel therapeutic approaches. Further studies are needed to differentiate the factors influencing the formation of bacterial endocarditis in biofilm deficient mutants of enterococci. Chitin is one of the most abundant biopolymer in nature and is made up of an insoluble homopolymer of b-1,4 linked N-acetyl glucosamine units. Chitin serves a morphological structural role in arthropods, including Procyanidin-B2 crustaceans and insects, as well as mollusks, nematodes, and worms. It is also found in fungi, making up from less than 1% to more than 40% of the cell wall, depending on the species.