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Interkingdom adenosine signal reduces Pseudomonas aeruginosa pathogenicity

Lili Sheng1, Mingming Pu, Manjunath Hegde

  • 1Department of Chemical Engineering, Texas A & M University, College Station, TX 77843-3122, USA.

Microbial Biotechnology
|March 15, 2012
PubMed

Insights

Adenosine, from host ATP, signals Pseudomonas aeruginosa in the gut. This signal significantly reduces biofilm formation and virulence factors, decreasing the pathogen

Area of Science:

  • Microbiology
  • Pathogen-host interactions
  • Gastrointestinal tract infections

Background:

  • Pseudomonas aeruginosa is an emerging pathogen in the gastrointestinal tract.
  • Host-derived molecules can act as signals influencing bacterial behavior and virulence.

Purpose of the Study:

  • To investigate the role of adenosine as an interkingdom signal for Pseudomonas aeruginosa in the GI tract.
  • To determine the impact of adenosine on P. aeruginosa biofilm formation, swarming motility, and virulence factor production.

Main Methods:

  • Treatment of P. aeruginosa with adenosine and its metabolite inosine.
  • Assessment of biofilm formation and swarming motility.
  • Quantification of virulence factors (pyocyanin, elastase, etc.).
  • Whole-transcriptome analysis to understand gene expression changes.
  • Virulence testing in Caenorhabditis elegans.

Main Results:

  • Adenosine significantly reduced P. aeruginosa biofilm formation and swarming motility by inhibiting rhamnolipid production.
  • Adenosine decreased the production of multiple virulence factors, including pyocyanin, elastase, and siderophores.
  • Whole-transcriptome analysis revealed that adenosine represses genes associated with iron acquisition, mimicking an iron-replete state.
  • Adenosine reduced P. aeruginosa virulence in C. elegans.

Conclusions:

  • Adenosine acts as a potent interkingdom signal in the GI tract, reducing P. aeruginosa pathogenicity.
  • The reduction in virulence is mediated by the repression of iron acquisition genes, independent of adenosine metabolism.
  • Understanding this host-pathogen communication can inform strategies to combat P. aeruginosa infections.

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