An examination of the role of disulfide bond isomerase a protein in bacterial virulence
3rd International Conference and Exhibition on Cell & Gene Therapy
October 27-29, 2014 Embassy Suites Las Vegas, USA

Sonal Malhotra

Scientific Tracks Abstracts: J Stem Cell Res Ther

Abstract:

In the last two decades there has been a tremendous increase in number of bacterial genome sequencing projects. This effort has yielded a large collection of data that is freely available to researchers. The role of this study to perform selective and informed literature searches to establish the role of disulfide isomerases from different organisms in virulence in their respective hosts. DsbA and DsbA-like proteins have been implicated in bacterial virulence for a long time. Recently DsbA proteins have been implicated in biofilm formation or maturation in several bacterial species. Biofilms are relevant to the medical community. In particular, Bacterial cells in biofilm exhibit altered resistance to antibiotics. Furthermore biofilms comprising mixed populations of different bacterial species have been demonstrated on medical implant devices. Therapeutic intervention on such medical implants has been attempted. Disruption of dsbA gene in P. aeruginosa leads to a reduction in virulence in an animal infection model. We have recently shown that a dsbA disruption in P. aeruginosa PAO1 exhibits enhanced biofilm formation with respect to the wild type strain. This result is similar to results with P. putida: where adsbA disruption exhibits enhanced exopolysachharide and biofilm formation. In our simple biofilm assay examining gross biofilm formation: The kinetics of biofilm formation on plastic (petri dish) and aluminum are higher in the dsbA mutant with respect to the wild type strain. The similarity in findings between P. aeruginosa and P. putida support the notion ofconservation in the mechanisms of biofilm formation amongst different bacterial species. This lends credence to examining biofilm formation pathways in different bacterial species. Such a study will likely reveal conservation in mechanisms of biofilm formation and maturation. It is likely to pave the way for potential avenues for further research and therapeutic intervention. We will report here in this study some some key players in biofilm formation and any likely conserved mechanisms of biofilm formation. Further studies are likely to support a comparison of biofilm formation in a plant infection model (Wt and dsbA disruption mutant) and evaluation of biofilm formation on different materials.