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Bae HJ, Yi H, Yoon SH, Koo BS, Kwon M, Cho JY, Lee CE, Hong S: Surfactin from Bacillus subtilis displays antiproliferative effect via apoptosis induction, cell cycle arrest and survival signaling www.selleckchem.com/products/H-89-dihydrochloride.html suppression. selleck screening library FEBS Lett 2007, 581:865–871.PubMedCrossRef 25. Koonin EV, Aravind L: Origin and evolution of eukaryotic apoptosis: the bacterial connection. Cell Death Differ 2002, 9:394–404.PubMedCrossRef 26. Hooper LV, Gordon JI: Commensal host-bacterial relationships in the gut. Science 2001, 292:1114–1118.CrossRef Authors’ contributions QG and JW participated in the design

of the experiment and its implementation, data analysis, and wrote the manuscript. LQ carried out Selleck BI 10773 bacteria culture, western blotting, real-time PCR and ELISA. TW was involved in the cell culture, SiRNA transient transfection, IL-10 neutralization, stimulation of cells, PI assay, Caspase-3 activity Galactosylceramidase assay and DNA fragmentation analyses. All authors have read and approved the final manuscript. The authors declare no conflict of interest.”
“Background In recent years, coagulase-negative Staphylococcus epidermidis ( Se)

has become the leading cause of infections related to indwelling medical devices such as vascular catheters, prosthetic joints and artificial heart valves [1, 2]. Pathogenicity of Se is attributed to its formation of biofilm on the surface of medical devices, thereby enhancing Se resistance to antibiotics and host defenses in this setting [3, 4]. In general, Se biofilm formation is a two-step process, in which bacteria first adhere to the surface (initial attachment phase) and subsequently form cell–cell aggregates and a multilayered architecture (accumulative phase) [5, 6]. One autolysin protein, AtlE, facilitates bacterial attachment to the surface of medical devices and dictates pathogenesis for Se biofilm-associated infections in vivo [7, 8]. In the accumulative phase, the polysaccharide intercellular adhesin (PIA), a linear poly-Nacetyl-1,6-β-glucosamine (PNAG) encoded by the icaADBC locus, is the major pathogenic determinant for intercellular adhesion [9, 10].