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A High-throughput, High-content, Liquid-based C. elegans Pathosystem
Published on: July 1, 2018
A Stenotrophomonas maltophilia Strain Evades a Major Caenorhabditis elegans Defense Pathway
Corin V White1, Brian J Darby1, Robert J Breeden1
1Ecological Genomics Institute, Division of Biology, Kansas State University, Manhattan, Kansas, USA.
Abstract:
Stenotrophomonas maltophilia is a ubiquitous bacterium and an emerging nosocomial pathogen. This bacterium is resistant to many antibiotics, associated with a number of infections, and a significant health risk, especially for immunocompromised patients. Given that Caenorhabditis elegans shares many conserved genetic pathways and pathway components with higher organisms, the study of its interaction with bacterial pathogens has biomedical implications. S. maltophilia has been isolated in association with nematodes from grassland soils, and it is likely that C. elegans encounters this bacterium in nature. We found that a local S. maltophilia isolate, JCMS, is more virulent than the other S. maltophilia isolates (R551-3 and K279a) tested. JCMS virulence correlates with intestinal distension and bacterial accumulation and requires the bacteria to be alive. Many of the conserved innate immune pathways that serve to protect C. elegans from various pathogenic bacteria also play a role in combating S. maltophilia JCMS. However, S. maltophilia JCMS is virulent to normally pathogen-resistant DAF-2/16 insulin-like signaling pathway mutants. Furthermore, several insulin-like signaling effector genes were not significantly differentially expressed between S. maltophilia JCMS and avirulent bacteria (Escherichia coli OP50). Taken together, these findings suggest that S. maltophilia JCMS evades the pathogen resistance conferred by the loss of DAF-2/16 pathway components. In summary, we have discovered a novel host-pathogen interaction between C. elegans and S. maltophilia and established a new animal model with which to study the mode of action of this emerging nosocomial pathogen.
Insights
Stenotrophomonas maltophilia is a dangerous nosocomial pathogen. This study reveals Caenorhabditis elegans as a new model to explore how S. maltophilia evades immune pathways, particularly the DAF-2/16 insulin-like signaling pathway.
Area of Science:
- Microbiology
- Pathogen Research
- Model Organism Studies
Background:
- Stenotrophomonas maltophilia is an emerging nosocomial pathogen known for antibiotic resistance and posing health risks, especially to immunocompromised individuals.
- Caenorhabditis elegans shares conserved genetic pathways with higher organisms, making it a valuable model for studying host-pathogen interactions with biomedical relevance.
- S. maltophilia has been found in soil environments where C. elegans resides, suggesting natural encounters between the bacterium and the nematode.
Purpose of the Study:
- To investigate the host-pathogen interaction between Caenorhabditis elegans and Stenotrophomonas maltophilia.
- To establish C. elegans as a model system for studying the virulence mechanisms of S. maltophilia.
- To explore how S. maltophilia JCMS interacts with C. elegans innate immunity and the DAF-2/16 insulin-like signaling pathway.
Main Methods:
- Comparative virulence assays using different S. maltophilia isolates (JCMS, R551-3, K279a) in C. elegans.
- Assessment of bacterial accumulation, intestinal distension, and requirement for live bacteria in pathogenesis.
- Analysis of C. elegans innate immune pathways, including the DAF-2/16 insulin-like signaling pathway and its effector genes, in response to S. maltophilia JCMS infection.
Main Results:
- A local S. maltophilia isolate (JCMS) demonstrated higher virulence in C. elegans compared to other isolates, characterized by intestinal distension and bacterial accumulation.
- JCMS virulence was dependent on live bacteria and engaged C. elegans innate immune pathways.
- S. maltophilia JCMS was virulent in normally resistant DAF-2/16 insulin-like signaling pathway mutants, suggesting evasion of this specific resistance mechanism.
- Key insulin-like signaling effector genes showed no significant differential expression during infection with virulent S. maltophilia JCMS compared to an avirulent control.
Conclusions:
- Caenorhabditis elegans serves as a novel and effective model for studying Stenotrophomonas maltophilia pathogenesis.
- S. maltophilia JCMS exhibits virulence by evading the pathogen resistance normally conferred by the DAF-2/16 insulin-like signaling pathway in C. elegans.
- This study establishes a new platform for dissecting the molecular mechanisms underlying S. maltophilia infections and antibiotic resistance.
