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The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions
Published on: October 18, 2017
Burkholderia pseudomallei kills the nematode Caenorhabditis elegans using an endotoxin-mediated paralysis
A L O'Quinn1, E M Wiegand, J A Jeddeloh
1Bacteriology Division, United States Army Medical Research Institute of Infectious Disease, 1425 Porter St., Fort Detrick, MD 21702-5011, USA.
Abstract:
We investigated a non-mammalian host model system for fitness in genetic screening for virulence-attenuating mutations in the potential biowarfare agents Burkholderia pseudomallei and Burkholderia mallei. We determined that B. pseudomallei is able to cause 'disease-like' symptoms and kill the nematode Caenorhabditis elegans. Analysis of killing in the surrogate disease model with B. pseudomallei mutants indicated that killing did not require lipopolysaccharide (LPS) O-antigen, aminoglycoside/macrolide efflux pumping, type II pathway-secreted exoenzymes or motility. Burkholderia thailandensis and some strains of Burkholderia cepacia also killed nematodes. Manipulation of the nematode host genotype suggests that the neuromuscular intoxication caused by both B. pseudomallei and B. thailandensis acts in part through a disruption of normal Ca2+ signal transduction. Both species produce a UV-sensitive, gamma-irradiation-resistant, limited diffusion, paralytic agent as part of their nematode pathogenic mechanism. The results of this investigation suggest that killing by B. pseudomallei is an active process in C. elegans, and that the C. elegans model might be useful for the identification of vertebrate animal virulence factors in B. pseudomallei.
Insights
The nematode Caenorhabditis elegans serves as a model for studying Burkholderia pseudomallei virulence. This research identified a paralytic agent involved in nematode killing, aiding biowarfare agent research.
Area of Science:
- Microbiology
- Pathogen Research
- Genetics
Background:
- Potential biowarfare agents Burkholderia pseudomallei and Burkholderia mallei pose significant threats.
- Genetic screening is crucial for identifying virulence-attenuating mutations in these pathogens.
- Non-mammalian host models offer a feasible alternative for studying virulence factors.
Purpose of the Study:
- To establish and validate a non-mammalian host model for genetic screening of virulence factors in Burkholderia species.
- To investigate the mechanism of pathogenesis of Burkholderia pseudomallei in a model organism.
Main Methods:
- Utilized the nematode Caenorhabditis elegans as a non-mammalian host model.
- Performed genetic screening using Burkholderia pseudomallei mutants.
- Analyzed nematode host genotype manipulation to understand intoxication mechanisms.
- Characterized the properties of the paralytic agent produced by the bacteria.
Main Results:
- Burkholderia pseudomallei effectively caused disease-like symptoms and mortality in Caenorhabditis elegans.
- Bacterial killing did not require lipopolysaccharide (LPS) O-antigen, specific efflux pumping, type II secreted exoenzymes, or motility.
- Burkholderia thailandensis and some Burkholderia cepacia strains also exhibited nematode-killing activity.
- Evidence suggests neuromuscular intoxication by B. pseudomallei and B. thailandensis involves disruption of calcium (Ca2+) signal transduction.
- A UV-sensitive, irradiation-resistant, limited-diffusion paralytic agent was identified as part of the pathogenic mechanism.
Conclusions:
- The Caenorhabditis elegans model is a viable system for studying Burkholderia virulence.
- Bacterial killing of nematodes is an active process mediated by specific factors.
- The identified paralytic agent and calcium signaling disruption are key to the nematode pathogenesis.
- This model system holds potential for identifying virulence factors relevant to vertebrate hosts.
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