Caenorhabditis elegans Slow Killing recapitulates chronic Pseudomonas aeruginosa infection and reveals mediators of host-pathogen interactions
- 1Department of BioSciences, Rice University
- 2Department of Bioengineering, Rice University
Abstract
Pseudomonas aeruginosa is a leading cause of healthcare-associated infections, especially in immunocompromised patients and individuals with cystic fibrosis (CF). P. aeruginosa commonly causes chronic infections within the respiratory tracts of patients with CF. These infections are marked by a shift from the production of acute virulence factors (secreted toxins) to colonization (biofilm formation) and persistence within the host. To better understand the transcriptomic changes that occur during this shift within the context of host-pathogen interactions, we took advantage of a whole-organism model system. Using an established Caenorhabditis elegans – P. aeruginosa colonization model, we identified genes differentially regulated during establishment of the infection of the C. elegans intestine. By comparing this transcriptomic signature to those from P. aeruginosa from CF sputum samples and an ex vivo porcine lung biofilm model, we demonstrated that Slow Killing partially recapitulates chronic lung infection. Notably, we observed the upregulation of lipid A and exopolysaccharide (Pel, alginate) biosynthetic genes within the nematode host and downregulation of acute virulence pathways including quorum-sensing, phenazine production, toxin secretion, and siderophore-mediated iron uptake. Further characterization of these differentially-regulated genes revealed key bacterial pathways, including quorum-sensing and the PhoPQ regulatory network, that impacted host survival during infection. These results demonstrate that the C. elegans Slow Killing model is a highly accessible tool for studying host-pathogen interactions and benchmark it against clinical samples.
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BibTeX
@article{gaskins2026caenorhabditis,
title = {{Caenorhabditis elegans Slow Killing recapitulates chronic Pseudomonas aeruginosa infection and reveals mediators of host-pathogen interactions}},
author = {Sadie Gaskins and Liyang Zhang and Donghoon Kang and Qi Xu and Natalia V. Kirienko},
journal = {Frontiers in Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fmicb.2026.1990701},
url = {https://www.frontiersin.org/articles/10.3389/fmicb.2026.1990701/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Caenorhabditis elegans Slow Killing recapitulates chronic Pseudomonas aeruginosa infection and reveals mediators of host-pathogen interactions
AU - Sadie Gaskins
AU - Liyang Zhang
AU - Donghoon Kang
AU - Qi Xu
AU - Natalia V. Kirienko
PY - 2026
DA - 2026/10/21
JO - Frontiers in Microbiology
DO - 10.3389/fmicb.2026.1990701
UR - https://www.frontiersin.org/articles/10.3389/fmicb.2026.1990701/full
AB - Pseudomonas aeruginosa is a leading cause of healthcare-associated infections, especially in immunocompromised patients and individuals with cystic fibrosis (CF). P. aeruginosa commonly causes chronic infections within the respiratory tracts of patients with CF. These infections are marked by a shift from the production of acute virulence factors (secreted toxins) to colonization (biofilm formation) and persistence within the host. To better understand the transcriptomic changes that occur during this shift within the context of host-pathogen interactions, we took advantage of a whole-organism model system. Using an established Caenorhabditis elegans – P. aeruginosa colonization model, we identified genes differentially regulated during establishment of the infection of the C. elegans intestine. By comparing this transcriptomic signature to those from P. aeruginosa from CF sputum samples and an ex vivo porcine lung biofilm model, we demonstrated that Slow Killing partially recapitulates chronic lung infection. Notably, we observed the upregulation of lipid A and exopolysaccharide (Pel, alginate) biosynthetic genes within the nematode host and downregulation of acute virulence pathways including quorum-sensing, phenazine production, toxin secretion, and siderophore-mediated iron uptake. Further characterization of these differentially-regulated genes revealed key bacterial pathways, including quorum-sensing and the PhoPQ regulatory network, that impacted host survival during infection. These results demonstrate that the C. elegans Slow Killing model is a highly accessible tool for studying host-pathogen interactions and benchmark it against clinical samples.
SN - 1664-302X
ER -