Killing of Caenorhabditis elegans by Pseudomonas aeruginosa used to model mammalian bacterial pathogenesis

Abstract

We show that a single clinical isolate of the human opportunistic pathogen Pseudomonas aeruginosa (strain PA14), which previously was shown to be pathogenic in mice and plants, also kills Caenorhabditis elegans. The rate of PA14-mediated killing of C. elegans depends on the composition of the agar medium on which PA14 is grown. When PA14 is grown on minimal medium, killing occurs over the course of several days and is referred to as ''slow'' killing. When PA14 is grown on high-osmolarity medium, killing occurs over the course of several hours and is referred to as ''fast'' killing. Several lines of evidence, including the fact that heat-killed bacteria are still capable of fast but not slow killing of C. elegans, indicate that fast and slow killing occur by distinct mechanisms. Slow killing involves an infection-like process and correlates with the accumulation of PA14 within worm intestines. Among 10 PA14 virulence-related mutants that had been shown previously to affect pathogenicity in plants and mice, 6 were less effective in killing C. elegans under both fastand slow-killing conditions, indicating a high degree of commonalty among the P. aeruginosa factors required for pathogenicity in disparate eukaryotic hosts. Thus, we show that a C. elegans pathogenicity model that is genetically tractable from the perspectives of both host and pathogen can be used to model mammalian bacterial pathogenesis.

Genome-wide analysis of DNA repeats in Burkholderia cenocepacia J2315 identifies a novel adhesin-like gene unique to epidemic-associated strains of the ET-12 lineage

“…We have observed that BCAM0224 gene expression elicited great changes for cells grown under environmental conditions that mimic the altered microenvironment of the CF lungs. Similar to our work, other studies on CF pathogens exposed to high osmolar conditions have shown a dramatic enhancement of the expression levels of other virulence genes, either from B. cenocepacia (Tomich & Mohr, 2004;Bhatt & Weingart, 2008) or Pseudomonas aeruginosa (Tan et al, 1999). Based on these observations, we speculate that expression of BCAM0224 may play a role in the virulence of B. cenocepacia when it infects CF patients.…”

Antimicrobial effectors in the nematode Caenorhabditis elegans : an outgroup to the Arthropoda

“…In the current review, we focus on the model nematode Caenorhabditis elegans, which has become a central model organism for studying the genetics of invertebrate immunity. First work in this field was published in 1999 [4,5]. Since then, the nematode's response to a variety of pathogens has been assessed.…”

Mathematical modeling of bacterial virulence and host–pathogen interactions in the Dictyostelium/Pseudomonas system

“…The C. elegans fast killing assays (Tan et al, 1999) Non-motile individuals were considered as dead, and the killing percentage was calculated as the ratio between dead and total C. elegans individuals.…”