BdlA, DipA and induced dispersion contribute to acute virulence and chronic persistence of Pseudomonas aeruginosa

PLoS Pathog. 2014 Jun 5;10(6):e1004168. doi: 10.1371/journal.ppat.1004168. eCollection 2014 Jun.

Abstract

The human pathogen Pseudomonas aeruginosa is capable of causing both acute and chronic infections. Differences in virulence are attributable to the mode of growth: bacteria growing planktonically cause acute infections, while bacteria growing in matrix-enclosed aggregates known as biofilms are associated with chronic, persistent infections. While the contribution of the planktonic and biofilm modes of growth to virulence is now widely accepted, little is known about the role of dispersion in virulence, the active process by which biofilm bacteria switch back to the planktonic mode of growth. Here, we demonstrate that P. aeruginosa dispersed cells display a virulence phenotype distinct from those of planktonic and biofilm cells. While the highest activity of cytotoxic and degradative enzymes capable of breaking down polymeric matrix components was detected in supernatants of planktonic cells, the enzymatic activity of dispersed cell supernatants was similar to that of biofilm supernatants. Supernatants of non-dispersing ΔbdlA biofilms were characterized by a lack of many of the degradative activities. Expression of genes contributing to the virulence of P. aeruginosa was nearly 30-fold reduced in biofilm cells relative to planktonic cells. Gene expression analysis indicated dispersed cells, while dispersing from a biofilm and returning to the single cell lifestyle, to be distinct from both biofilm and planktonic cells, with virulence transcript levels being reduced up to 150-fold compared to planktonic cells. In contrast, virulence gene transcript levels were significantly increased in non-dispersing ΔbdlA and ΔdipA biofilms compared to wild-type planktonic cells. Despite this, bdlA and dipA inactivation, resulting in an inability to disperse in vitro, correlated with reduced pathogenicity and competitiveness in cross-phylum acute virulence models. In contrast, bdlA inactivation rendered P. aeruginosa more persistent upon chronic colonization of the murine lung, overall indicating that dispersion may contribute to both acute and chronic infections.

Publication types

  • Comparative Study

MeSH terms

  • Acute Disease
  • Animals
  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism*
  • Biofilms / growth & development*
  • Cells, Immobilized / enzymology
  • Cells, Immobilized / physiology
  • Chronic Disease
  • Gene Deletion
  • Gene Expression Regulation, Bacterial*
  • Host-Pathogen Interactions
  • Lung / microbiology
  • Mice
  • Microbial Interactions
  • Opportunistic Infections / microbiology
  • Phosphoric Diester Hydrolases / genetics
  • Phosphoric Diester Hydrolases / metabolism*
  • Plankton / growth & development
  • Plankton / pathogenicity
  • Plankton / physiology
  • Pneumonia, Bacterial / microbiology*
  • Pseudomonas Infections / microbiology*
  • Pseudomonas aeruginosa / enzymology
  • Pseudomonas aeruginosa / growth & development
  • Pseudomonas aeruginosa / pathogenicity
  • Pseudomonas aeruginosa / physiology*
  • Virulence
  • Virulence Factors / genetics
  • Virulence Factors / metabolism

Substances

  • Bacterial Proteins
  • Virulence Factors
  • Phosphoric Diester Hydrolases

Grants and funding

This work was supported by a grant from NIH (1RO1 A107525701A2). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.