title: Involvement of nitric oxide in biofilm dispersal of Pseudomonas aeruginosa.
abstract: Bacterial biofilms at times undergo regulated and coordinated dispersal events where sessile biofilm cells convert to free-swimming, planktonic bacteria. In the opportunistic pathogen Pseudomonas aeruginosa, we previously observed that dispersal occurs concurrently with three interrelated processes within mature biofilms: (i) production of oxidative or nitrosative stress-inducing molecules inside biofilm structures, (ii) bacteriophage induction, and (iii) cell lysis. Here we examine whether specific reactive oxygen or nitrogen intermediates play a role in cell dispersal from P. aeruginosa biofilms. We demonstrate the involvement of anaerobic respiration processes in P. aeruginosa biofilm dispersal and show that nitric oxide (NO), used widely as a signaling molecule in biological systems, causes dispersal of P. aeruginosa biofilm bacteria. Dispersal was induced with low, sublethal concentrations (25 to 500 nM) of the NO donor sodium nitroprusside (SNP). Moreover, a P. aeruginosa mutant lacking the only enzyme capable of generating metabolic NO through anaerobic respiration (nitrite reductase, DeltanirS) did not disperse, whereas a NO reductase mutant (DeltanorCB) exhibited greatly enhanced dispersal. Strategies to induce biofilm dispersal are of interest due to their potential to prevent biofilms and biofilm-related infections. We observed that exposure to SNP (500 nM) greatly enhanced the efficacy of antimicrobial compounds (tobramycin, hydrogen peroxide, and sodium dodecyl sulfate) in the removal of established P. aeruginosa biofilms from a glass surface. Combined exposure to both NO and antimicrobial agents may therefore offer a novel strategy to control preestablished, persistent P. aeruginosa biofilms and biofilm-related infections.
authors.affiliation: School of Biotechnology and Biomolecular Sciences and Centre for Marine Biofouling and Bio-innovation, Biological Sciences Building, University of New South Wales, Kensington, Sydney, NSW 2052, Australia.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Barraud
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Hassett
authors.forename: Sung-Hei
authors.initials: SH
authors.lastname: Hwang
authors.forename: Scott A
authors.initials: SA
authors.lastname: Rice
authors.forename: Staffan
authors.initials: S
authors.lastname: Kjelleberg
authors.forename: Jeremy S
authors.initials: JS
authors.lastname: Webb
mesh_terms: D000222:Adaptation, Physiological; D000693:Anaerobiosis; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D018441:Biofilms / Q000187:drug effects; D015169:Colony Count, Microbial; D004357:Drug Synergism; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008856:Microscopy, Fluorescence; D009068:Movement; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009572:Nitrite Reductases / Q000235:genetics; D009599:Nitroprusside / Q000494:pharmacology; D010088:Oxidoreductases / Q000235:genetics; D011550:Pseudomonas aeruginosa / Q000187:drug effects / Q000502:physiology*; D012967:Sodium Dodecyl Sulfate / Q000494:pharmacology; D014031:Tobramycin / Q000494:pharmacology
chemical_list: D000900:Anti-Bacterial Agents; D020030:Nitric Oxide Donors; D009599:Nitroprusside; D009569:Nitric Oxide; D012967:Sodium Dodecyl Sulfate; D006861:Hydrogen Peroxide; D010088:Oxidoreductases; D009572:Nitrite Reductases; C034747:nitric-oxide reductase; D014031:Tobramycin