Most recent global transcription and proteomic profiling has revealed several aspects of the physiological adaptations that S. mutans undergoes following attachment to and growth on surfaces [21, 36–38]. Nevertheless, only a few comprehensive studies have compared the influence of surface materials on the gene expression of immobilized bacteria adhering to different dental biomaterials.

It is conceivable that the chemistry of the surface on which the biofilm is formed would affect the properties of the biofilm. Recent gene expression profiling showed marked differences in gene responses of bone cells on smooth and rough titanium surfaces [39]. Additional studies demonstrated that the biodegradation PLX3397 purchase of composite resins differentially impacts the growth and gene expression of S. mutans [40]. In addition, buy P005091 biomaterial surface chemistry affected biofilm formation, and polyethylene oxide significantly inhibited S. epidermidis biofilm formation in vitro [41]. In the current study, we have shown that gene expression differs in S. mutans biofilms formed on different surfaces, therefore likely changing the physiology and virulence of the immobilized bacteria. Our CLSM biofilm depth analysis shows that the bacteria were able to construct more confluent and thick biofilms on a hydroxyapatite surface compared

to the other surfaces tested. AI-2 is a furanone borate diester that is synthesized in many bacteria by the LuxS protein and detected in Vibrio harveyi by a periplasmic protein called LuxP. It was proposed to function as a universal quorum-sensing signal for interaction between different bacterial species [42]. It has been previously shown that the AI-2 level decreased in chemostat-grown E. coli cultures exposed to different stresses [43]. In addition, QS is likely involved in stress gene regulation in Porphyromonas gingivalis [44]. The www.selleck.co.jp/products/cobimetinib-gdc-0973-rg7420.html consequences

of these data may provide the potential link between the type of surface, QS and stress regulation in biofilm-grown bacteria. This might suggest that the attachment of bacteria to a particular surface may have altered the level of AI-2 signaling in the generated biofilm to overcome stressful conditions. Consistent with this hypothesis is that the levels of AI-2 in biofilms from various I-BET-762 concentration tested surfaces were found to be different (Figure 5). The stressful situation during the transition to a new surface apparently induces the bacteria to enhance the QS process to overcome the challenge by activating stress-related as well as biofilm-associated genes at the same time. Although small peptides termed competence stimulating peptides (CSP) are the main QS signaling molecules in S. mutans [45], It was shown that AI-2produced by S. mutans play a role in biofilm formation [27] and analogues of the AI-2 may affect biofilm formation of S. mutans [46]. Moreover, secretion of AI-2 of S.

Besides immune escape and nutrient acquisition, our results reveal another area, where these Gram-negative pathogens employ species-specific

pathogenicity factors. Clearly, adhesion to the mucosal surface epithelium is the initial step in the colonization by CEACAM-binding bacteria, and the possession of adhesive proteins specifically targeting human CEACAMs might promote this step. However, at the same time this specialization could contribute to the limited host spectrum not only of pathogenic Neisseriae, but also of M. catarrhalis and Haemophilus influenzae. Conclusions Recognition of host surface structures is critical for many bacterial pathogens to establish a first foothold in their target organism. Whereas a high degree of specificity might allow intimate binding of the microorganisms to eukaryotic cells, it might at the same time limit the host range of the pathogen. Here we reveal a selective interaction between bacteria NSC23766 and the human form of the cell surface receptor CEACAM1 that correlates with the human-restricted pathogenicity of

these microbes. Our analysis not only points to an ongoing pathogen-host co-evolution at the level of receptor-adhesin interaction, but further strengthens the idea that the OpaCEA protein-mediated Emricasan solubility dmso interaction with human CEACAMs might provide an access point for preventing or limiting infection. Acknowledgements We thank M. Frosch (Universität Würzburg, Germany) and T.F. Meyer (Max-Planck-Institute für Infektionsbiologie, Berlin, Germany) for the bacterial strains used in this study. We thank D.W. Piston (Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN) for Cerulean cDNA, S. Feindler-Boeckh and R. Hohenberger-Bregger for expert technical assistance. MV and CRH acknowledge the support by the Konstanz Research School-Chemical Biology. This study was supported

by funds from the DFG (Ha2856/6-1) to C.R.H. References 1. Hammarstrom heptaminol S: The carcinoembryonic antigen (CEA) family: structures, suggested functions and expression in normal and malignant tissues. Semin Cancer Biol 1999, 9:67–81.PubMedCrossRef 2. Zebhauser R, Kammerer R, Eisenried A, McLellan A, Moore T, Zimmermann W: Identification of a novel group of evolutionarily conserved members within the rapidly diverging murine Cea family. Genomics 2005, 86:566–580.PubMedCrossRef 3. Kammerer R, Popp T, Hartle S, Singer BB, Zimmermann W: Species-specific evolution of immune receptor tyrosine based activation motif-containing CEACAM1-related immune receptors in the dog. BMC Evol Biol 2007, 7:196.PubMedCrossRef 4. Kammerer R, Zimmermann W: Coevolution of activating and inhibitory receptors within mammalian carcinoembryonic antigen (CEA) families. BMC Biology 2010, 8:12.PubMedCrossRef 5. Kammerer R, Popp T, Singer BB, Schlender J, Zimmermann W: Identification of allelic variants of the this website bovine immune regulatory molecule CEACAM1 implies a pathogen-driven evolution.