ArticleBMC microbiology2020
Identification and characterization of differentially expressed genes in Caenorhabditis elegans in response to pathogenic and nonpathogenic Stenotrophomonas maltophilia.
Article in BMC microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- From nature to clinic: tracking genetic and environmental drivers of Stenotrophomonas maltophilia pathogenicity.Archives of microbiology · 2026Review
- Effects of a High-Glucose Diet onACS omega · 2026Article
- MAPK/PMK-1 innate immune signaling protects the nematode Caenorhabditis elegans from increased intestinal colonization in an animal host-pathogen model in space.NPJ microgravity · 2026Article
- Host TGF-β signalling facilitates Vi-capsule mediated adaptive immune evasion and vertical transmission ofCell surface (Amsterdam, Netherlands) · 2025Article
- Caenorhabditis elegans microbiome members have combinatorial effects on host survival and fitness.Scientific reports · 2025Article
- RiboTRAP-seq identifies spatially distinct functions for the anterior and posterior intestine in immune and metabolic regulation inbioRxiv : the preprint server for biology · 2025Article
- Identification of healthspan-promoting genes in Caenorhabditis elegans based on a human GWAS study.Biogerontology · 2022Article
- Article
- Take a Walk to the Wild Side ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- DietaryGut microbesArticle
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2 authors.
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Abstract
backgroundStenotrophomonas maltophilia is an emerging nosocomial pathogen that causes infection in immunocompromised patients. S. maltophilia isolates are genetically diverse, contain diverse virulence factors, and are variably pathogenic within several host species. Members of the Stenotrophomonas genus are part of the native microbiome of C. elegans, being found in greater relative abundance within the worm than its environment, suggesting that these bacteria accumulate within C. elegans. Thus, study of the C. elegans-Stenotrophomonas interaction is of both medical and ecological significance. To identify host defense mechanisms, we analyzed the C. elegans transcriptomic response to S. maltophilia strains of varying pathogenicity: K279a, an avirulent clinical isolate, JCMS, a virulent strain isolated in association with soil nematodes near Manhattan, KS, and JV3, an even more virulent environmental isolate.
resultsOverall, we found 145 genes that are commonly differentially expressed in response to pathogenic S. maltophilia strains, 89% of which are upregulated, with many even further upregulated in response to JV3 as compared to JCMS. There are many more JV3-specific differentially expressed genes (225, 11% upregulated) than JCMS-specific differentially expressed genes (14, 86% upregulated), suggesting JV3 has unique pathogenic mechanisms that could explain its increased virulence. We used connectivity within a gene network model to choose pathogen-specific and strain-specific differentially expressed candidate genes for functional analysis. Mutations in 13 of 22 candidate genes caused significant differences in C. elegans survival in response to at least one S. maltophilia strain, although not always the strain that induced differential expression, suggesting a dynamic response to varying levels of pathogenicity.
conclusionsVariation in observed pathogenicity and differences in host transcriptional responses to S. maltophilia strains reveal that strain-specific mechanisms play important roles in S. maltophilia pathogenesis. Furthermore, utilizing bacteria closely related to strains found in C. elegans natural environment provides a more realistic interaction for understanding host-pathogen response.
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