title: Differential potentiation of the virulence of the Pseudomonas aeruginosa cystic fibrosis liverpool epidemic strain by oral commensal Streptococci.
abstract: BACKGROUND
  The Pseudomonas aeruginosa Liverpool epidemic strain (LES) is an important cystic fibrosis (CF) pathogen and is associated with increased morbidity and a worsened prognosis, compared with other CF-associated strains. However, interactions of common LES phenotypic variants with other members of the polymicrobial biofilms associated with chronic CF respiratory disease, such as oral commensal streptococci, have not been investigated.
  
  
  METHODS
  Biofilm population dynamics, virulence factor production, and pathogenicity in Galleria mellonella larvae of common LES phenotypes (ie, low production, intermediate production, and overproduction of pyocyanin) in the presence or absence of anginosus group streptococci (AGS) were compared.
  
  
  RESULTS
  AGS populations isolated from biofilm cocultures were P. aeruginosa phenotypic variant dependent, with higher AGS cell densities than those in monoculture frequently observed. Coexistence of AGS with a producer of low or intermediate levels of pyocyanin was found to result in enhancement of virulence factor production. In addition, the LES formed pathogenic partnerships with AGS in the G. mellonella infection model, with killing dependent on LES phenotype and AGS species.
  
  
  CONCLUSIONS
  The pathogenic potential of LES phenotypic variants can be enhanced by the presence of oral commensal streptococci. As adaptive mutations leading to reduced virulence factor production are commonplace, the observations made are relevant in the general context of the biology of P. aeruginosa infection during CF.
authors.affiliation: Department of Clinical and Diagnostic Oral Sciences, Institute of Dentistry.
authors.forename: Robert A
authors.initials: RA
authors.lastname: Whiley
authors.forename: Nargis P
authors.initials: NP
authors.lastname: Sheikh
authors.forename: Naseem
authors.initials: N
authors.lastname: Mushtaq
authors.forename: Eleni
authors.initials: E
authors.lastname: Hagi-Pavli
authors.forename: Yoann
authors.initials: Y
authors.lastname: Personne
authors.forename: Danish
authors.initials: D
authors.lastname: Javaid
authors.forename: Richard D
authors.initials: RD
authors.lastname: Waite
mesh_terms: D000818:Animals; D018441:Biofilms / Q000254:growth & development; D002460:Cell Line; D003550:Cystic Fibrosis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D058872:Epidemics; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D006801:Humans; D016209:Interleukin-8 / Q000276:immunology; D007814:Larva / Q000276:immunology / Q000382:microbiology; D009036:Moths / Q000276:immunology / Q000382:microbiology; D010196:Pancreatic Elastase / Q000276:immunology; D010641:Phenotype; D011552:Pseudomonas Infections / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D011550:Pseudomonas aeruginosa / Q000276:immunology*; D011710:Pyocyanine / Q000276:immunology; D013290:Streptococcal Infections / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D013291:Streptococcus / Q000276:immunology*; D014774:Virulence / Q000276:immunology*; D037521:Virulence Factors / Q000276:immunology
chemical_list: D016209:Interleukin-8; D037521:Virulence Factors; D011710:Pyocyanine; D010196:Pancreatic Elastase
keywords: Anginosus group streptococci; Galleria mellonella; IL-8; Pseudomonas aeruginosa; biofilm; virulence