Stress response of Pseudomonas aeruginosa to sodium hypochlorite leads to enhanced biofilm formation

  • chair:

    Strempel, N. / Strehmel, J. / Bugert, B. / Overhage, J. (2011)

  • place:

    How Dead is Dead 2011, Tübingen, Deutschland, 16.-17. Juni, 2011

  • Date: 2011
  • Strempel, N. / Strehmel, J. / Bugert, B. / Overhage, J. (2011): „Stress response of Pseudomonas aeruginosa to sodium hypochlorite leads to enhanced biofilm formation“. In: How Dead is Dead 2011, Tübingen, Deutschland, 16.-17. Juni, 2011

Abstract

Pseudomonas aeruginosa is a ubiquitous motile Gram-negative bacterium that plays an important role as an opportunistic pathogen in infectious diseases. Due to the size and complexity of its genome as well as the sophisticated and coordinated regulation of gene expression this bacterium is able to adapt to a variety of environments.

Since it has been shown recently that P. aeruginosa forms resistant biofilms in order to survive stressful environmental conditions e.g. growth in the presence of antimicrobial agents, the aim of this study was to investigate the stress response of P. aeruginosa PAO1 to the frequently used disinfectant sodium hypochlorite. Bacterial growth of P. aeruginosa PAO1 and biofilm formation in the presence of free chlorine at different concentrations were analyzed.

In order to identify the molecular mechanisms and regulating genes involved in the stress response to sodium hypochlorite, microarray analyses and follow up experiments were performed. In static attachment assays free chlorine at subinhibitory concentrations of 2 µg/ml led to a two-fold increase in early biofilm formation after two hours of incubation compared to the non-treated controls.

The altered biofilm structure and composition caused by sodium hypochlorite treatment was further studied by fluorescence microscopy under static conditions as well as in continuous flow cell experiments. Here we demonstrate that sublethal concentrations of sodium hypochlorite induce biofilm formation in P. aeruginosa PAO1 as a consequence of bacterial stress response to this important biocide.