faecium is able to adhere to human and mouse intestinal mucus in vitro and becomes associated in vivo with selleck inhibitor the intestinal mucus layer of clindamycin treated mice [37–39]. This suggests an interaction

between the bacterium and the mucus or with the epithelium itself. To examine the role of Esp in intestinal adherence and colonization, an Esp expressing strain of E. faecium (E1162) and its isogenic Esp-deficient mutant (E1162Δesp) were studied for adherence to differentiated Caco-2 cells and colonization of murine intestines. E1162, a hospital-acquired strain, exhibited significantly higher adherence to Caco-2 cells than E135, a representative of the indigenous flora. These results are consistent with an earlier study performed by Lund et al. [23]. However, no difference in adherence to Caco-2 cells between the E1162 and the E1162Δesp was found, indicating that Esp is not the determining factor responsible for the observed difference in Caco-2 cell adherence between nosocomial and indigenous E. faecium strains. This also implies that other determinants present in hospital-acquired

E. faecium strains contribute to adhesion to intestinal epithelial cells. Comparative this website genomic hybridizations of 97 E. faecium nosocomial, commensal and animal isolates identified more than 100 genes that were enriched in nosocomial strains, including genes encoding putative adhesins, antibiotic resistance, IS elements, phage sequences, and novel metabolic pathways [40]. In addition, similar Selleckchem Combretastatin A4 levels of intestinal

colonization or translocation were found after inoculation with E1162 wild type or the isogenic Esp mutant E1162Δesp. These data are in accordance with a study performed by Pultz et al. [27] in which they showed that Esp did not 4-Aminobutyrate aminotransferase facilitate intestinal colonization or translocation of E. faecalis in clindamycin-treated mice. Only from the small bowel contents of mice when inoculated separately with E1162 wild type and the Esp-mutant strain significantly more E1162Δesp compared to E1162 was isolated. This was an unexpected observation and we have no explanation for the fact that the levels of E1162Δesp in the small bowel are as high as in the cecum. Relatively lower levels as seen for E1162 are more typical for the small bowel. Conclusion Our data clearly demonstrate that Esp is not essential for high density colonization of the GI tract by nosocomial strains. Other possible candidate traits implicated in this process could include novel adhesins, like the novel cell surface proteins recently identified [41], bacteriocins, factors that resist specific or non-specific host defence mechanisms, and/or the ability to utilize new growth substrates. It is interesting in this respect that we recently identified a novel genomic island highly specific for nosocomial strains that tentatively encodes novel sugar uptake system [42]. For nosocomial E.