3B and C). Although S-IgA in saliva may not obtain access to bacteria accumulated within gum pockets, it is worth investigating click here whether S-IgA can eliminate the halitosis generated from plaque biofilms on the surface of mouse incisors and/or oral epithelium. Furthermore, since both IgG in serum and S-IgA in saliva were measurable in FomA-immunized mice, determination of other IgG subclasses (such as IgG1 and IgG2a) [25] and cell-mediated immunity may increase understanding of the potency of FomA-targeted vaccines. A qualitative

and quantitative examination of biofilm formation in vivo is still a challenge. Recently, a novel combination of measurements using an integrated nuclear magnetic resonance and confocal laser scanning microscope have been developed to study the processes occurring within biofilm communities [52]. These techniques may provide new tools for evaluation of the effects of vaccination on biofilm formation in vivo. Overall, we have demonstrated that FomA is a necessary component for co-aggregation of F. nucleatum with P. gingivalis. Bacterial co-aggregation

resulted in an enhancement of biofilm formation and VSC production in vitro and gum inflammation in vivo. Blocking FomA with a neutralizing antibody RG7204 mouse significantly attenuated this enhancement. Vaccination targeting FomA effectively suppressed co-infection-induced gum swelling and the production of MIP-2 cytokine. These results strongly suggested that FomA is critical mediator for bacterial co-aggregation and its associated pathogenicities. Inhibition of co-aggregation by inactivation of F. nucleatum FomA will prevent the inhibitors progress of oral infections at an early stage. F. nucleatum and P. gingivalis have been implicated in the pathogenesis of several diseases [5], including urinary tract infections, bacteremia, pericarditis, and disorders of the oral cavity much such as pulpal infections,

alveolar bone abscesses, periodontal disease and halitosis. The immunization approach developed in this study will benefit patients with diseases mentioned above. Most importantly, the concept of blocking bacterial co-aggregation and biofilm formation forms a model system for the study of other biofilm-related pathogenic phenotypes, including those that develop in skin ulcers and other chronic infections. This work was supported by National Institutes of Health Grants (R01-AI067395-01, R21-R022754-01, R21-I58002-01 and 1R41AR056169-01). We thank Dan MacLeod for critical review. “
“The authors would like to apologise for an error appearing in Fig. 4A in their paper. The correct version of the figure appears below. “
“Rather than pVenv4, a pSC11-based plasmid was used that encoded a lengthier BH10 envelope sequence. The predicted envelope sequence encoded by this construct extended to amino acid position 723 (based on the nomenclature of Owens et. al., J. Virol. 68 (1994) 570–574), and was followed by amino acids GDPTGPKE at the C terminus.