scholarly journals Caenorhabditis elegans responses to bacteria from its natural habitats

2016 ◽  
Vol 113 (27) ◽  
pp. E3941-E3949 ◽  
Author(s):  
Buck S. Samuel ◽  
Holli Rowedder ◽  
Christian Braendle ◽  
Marie-Anne Félix ◽  
Gary Ruvkun

Most Caenorhabditis elegans studies have used laboratory Escherichia coli as diet and microbial environment. Here we characterize bacteria of C. elegans' natural habitats of rotting fruits and vegetation to provide greater context for its physiological responses. By the use of 16S ribosomal DNA (rDNA)-based sequencing, we identified a large variety of bacteria in C. elegans habitats, with phyla Proteobacteria, Bacteroidetes, Firmicutes, and Actinobacteria being most abundant. From laboratory assays using isolated natural bacteria, C. elegans is able to forage on most bacteria (robust growth on ∼80% of >550 isolates), although ∼20% also impaired growth and arrested and/or stressed animals. Bacterial community composition can predict wild C. elegans population states in both rotting apples and reconstructed microbiomes: alpha-Proteobacteria-rich communities promote proliferation, whereas Bacteroidetes or pathogens correlate with nonproliferating dauers. Combinatorial mixtures of detrimental and beneficial bacteria indicate that bacterial influence is not simply nutritional. Together, these studies provide a foundation for interrogating how bacteria naturally influence C. elegans physiology.

2021 ◽  
Vol 9 (2) ◽  
pp. 310
Author(s):  
Masayuki Hashimoto ◽  
Yi-Fen Ma ◽  
Sin-Tian Wang ◽  
Chang-Shi Chen ◽  
Ching-Hao Teng

Uropathogenic Escherichia coli (UPEC) is a major bacterial pathogen that causes urinary tract infections (UTIs). The mouse is an available UTI model for studying the pathogenicity; however, Caenorhabditis elegans represents as an alternative surrogate host with the capacity for high-throughput analysis. Then, we established a simple assay for a UPEC infection model with C. elegans for large-scale screening. A total of 133 clinically isolated E. coli strains, which included UTI-associated and fecal isolates, were applied to demonstrate the simple pathogenicity assay. From the screening, several virulence factors (VFs) involved with iron acquisition (chuA, fyuA, and irp2) were significantly associated with high pathogenicity. We then evaluated whether the VFs in UPEC were involved in the pathogenicity. Mutants of E. coli UTI89 with defective iron acquisition systems were applied to a solid killing assay with C. elegans. As a result, the survival rate of C. elegans fed with the mutants significantly increased compared to when fed with the parent strain. The results demonstrated, the simple assay with C. elegans was useful as a UPEC infectious model. To our knowledge, this is the first report of the involvement of iron acquisition in the pathogenicity of UPEC in a C. elegans model.


Author(s):  
Rui Han ◽  
Yu Wang ◽  
Yang Deng ◽  
Yuqin Zhang ◽  
Lin Zhang ◽  
...  

AbstractThe soil-dwelling, opportunistic pathogenic bacterium "Bacillus nematocida" B16 exhibits strong killing activities against a variety of pathogenic nematodes via a “Trojan horse” mechanism that can kill worm species like Caenorhabditis elegans. The bacterial strain CPCC 101271 was previously isolated from the intestines of C. elegans that were recovered from natural habitats and can serve as a probiotic for C. elegans, while also assisting in resistance to infection by the pathogenic strain B16. In this study, the lifespan of C. elegans fed with strain CPCC 101271 cells was extended by approximately 40% compared with that of worms fed with Escherichia coli OP50 cells. In addition, the colonization of C. elegans by the pathogenic bacterium "B. nematocida" B16 was inhibited when pre-fed with strain CPCC 101271. Metagenomic sequence analysis of intestinal microbiota of C. elegans fed with strain CPCC 101271 and infected with B16 revealed that pre-feeding worms with CPCC 101271 improved the diversity of the intestinal bacteria. Moreover, community structure significantly varied in coordination with Stenotrophomonas spp. and Bacillus spp. abundances when competition between strains CPCC 101271 and B16 was evaluated. In conclusion, the nematode microbiota strain CPCC 101271 assisted in its host resistance to colonization by the pathogen "Bacillus nematocida" and can also promote life span-prolongation in C. elegans. These results underscore that understanding the interactions between C. elegans microbiota and pathogens can provide new insights into achieving effective biological control of agricultural pests.


2010 ◽  
Vol 78 (9) ◽  
pp. 4068-4076 ◽  
Author(s):  
Jennifer Hwang ◽  
Lisa M. Mattei ◽  
Laura G. VanArendonk ◽  
Philip M. Meneely ◽  
Iruka N. Okeke

ABSTRACT Enteroaggregative Escherichia coli (EAEC) strains are important diarrheal pathogens. EAEC strains are defined by their characteristic stacked-brick pattern of adherence to epithelial cells but show heterogeneous virulence and have different combinations of adhesin and toxin genes. Pathoadaptive deletions in the lysine decarboxylase (cad) genes have been noted among hypervirulent E. coli subtypes of Shigella and enterohemorrhagic E. coli. To test the hypothesis that cad deletions might account for heterogeneity in EAEC virulence, we developed a Caenorhabditis elegans pathogenesis model. Well-characterized EAEC strains were shown to colonize and kill C. elegans, and differences in virulence could be measured quantitatively. Of 49 EAEC strains screened for lysine decarboxylase activity, 3 tested negative. Most notable is isolate 101-1, which was recovered in Japan, from the largest documented EAEC outbreak. EAEC strain 101-1 was unable to decarboxylate lysine in vitro due to deletions in cadA and cadC, which, respectively, encode lysine decarboxylase and a transcriptional activator of the cadAB genes. Strain 101-1 was significantly more lethal to C. elegans than control strain OP50. Lethality was attenuated when the lysine decarboxylase defect was complemented from a multicopy plasmid and in single copy. In addition, restoring lysine decarboxylase function produced derivatives of 101-1 deficient in aggregative adherence to cultured human epithelial cells. Lysine decarboxylase inactivation is pathoadapative in an important EAEC outbreak strain, and deletion of cad genes could produce hypervirulent EAEC lineages in the future. These results suggest that loss, as well as gain, of genetic material can account for heterogeneous virulence among EAEC strains.


2021 ◽  
Author(s):  
Rui Han ◽  
Yu Wang ◽  
Yang Deng ◽  
Yuqin Zhang ◽  
Lin Zhang ◽  
...  

Abstract The soil-dwelling opportunistic bacterium Bacillus nematocida B16 shows comparatively strong killing activities against a variety of pathogenic nematodes. A bacterial strain CPCC 101271T, isolated from intestines of C. elegans in natural habitats, was found not only to be probiotics for C. elegans but also assist in resisting pathogen B16 infection. The lifespan of Caenorhabditis elegans fed on strain CPCC 101271T was extended by approximately 40% compared with that of worms fed on Escherichia coli OP50. In addition, the colonization of C. elegans by the pathogenic bacterium B. nematocida B16 was inhibited when it was pre-fed with strain CPCC 101271T. Based on a polyphasic taxonomy study including genotypic, chemotaxonomic and phenotypic characteristics, we propose that strain CPCC 101271T represents a novel bacterial species with the name Stenotrophomonas nematodicola sp. nov. and CPCC 101271T as the type strain. Metagenomic sequence analysis of the intestinal microbiota of C. elegans fed with strain CPCC 101271T and then infected with B16 revealed that pre-feeding with CPCC 101271T improved the diversity of intestinal bacteria, while the community structure varied significantly together with the fluctuation of Stenotrophomonas spp. and Bacillus spp. abundance during competition between strain CPCC 101271T and B16. In conclusion, the nematode microbiota strain CPCC 101271T, a novel species of the genus Stenotrophomonas, assisted in its host resistance to the pathogen Bacillus nematocida colonization, so as to act as an intestinal life span-prolonging for C. elegans.


Author(s):  
Joshua D. Brycki ◽  
Jeremy R. Chen See ◽  
Gillian R. Letson ◽  
Cade S. Emlet ◽  
Lavinia V. Unverdorben ◽  
...  

Previous research has reported effects of the microbiome on health span and life span of Caenorhabditis elegans , including interactions with evolutionarily conserved pathways in humans. We build on this literature by reporting the gene expression of Escherichia coli OP50 in wild-type (N2) and three long-lived mutants of C. elegans .


Nematology ◽  
2007 ◽  
Vol 9 (1) ◽  
pp. 87-91 ◽  
Author(s):  
James McGhee ◽  
Shervin Ghafouri

AbstractWe fed adult Caenorhabditis elegans fluorescent microspheres mixed with their Escherichia coli food and then measured the total fluorescence of expelled faeces as a function of time after transfer to unlabelled bacteria. Intestinal clearance obeys a simple first-order decay or dilution curve: we estimate that 43 ± 10% of the maximum intestinal volume is expelled in each defecation and the average residence time of a bead (by inference, a bacterium) is less than 2 min. Our results raise questions how bacteria can be sufficiently digested in this brief period to provide energy and material to sustain the high rate of C. elegans oocyte production.


2013 ◽  
Vol 79 (7) ◽  
pp. 2435-2445 ◽  
Author(s):  
Alexandra Merkx-Jacques ◽  
Anja Coors ◽  
Roland Brousseau ◽  
Luke Masson ◽  
Alberto Mazza ◽  
...  

ABSTRACTThe detection and abundance ofEscherichia coliin water is used to monitor and mandate the quality of drinking and recreational water. Distinguishing commensal waterborneE. coliisolates from those that cause diarrhea or extraintestinal disease in humans is important for quantifying human health risk. A DNA microarray was used to evaluate the distribution of virulence genes in 148E. colienvironmental isolates from a watershed in eastern Ontario, Canada, and in eight clinical isolates. Their pathogenic potential was evaluated withCaenorhabditis elegans, and the concordance between the bioassay result and the pathotype deduced by genotyping was explored. Isolates identified as potentially pathogenic on the basis of their complement of virulence genes were significantly more likely to be pathogenic toC. elegansthan those determined to be potentially nonpathogenic. A number of isolates that were identified as nonpathogenic on the basis of genotyping were pathogenic in the infection assay, suggesting that genotyping did not capture all potentially pathogenic types. The detection of the adhesin-encoding genessfaD,focA, andfocG, which encode adhesins; ofiroN2, which encodes a siderophore receptor; ofpic, which encodes an autotransporter protein; and ofb1432, which encodes a putative transposase, was significantly associated with pathogenicity in the infection assay. Overall,E. coliisolates predicted to be pathogenic on the basis of genotyping were indeed so in theC. elegansinfection assay. Furthermore, the detection ofC. elegans-infective environmental isolates predicted to be nonpathogenic on the basis of genotyping suggests that there are hitherto-unrecognized virulence factors or combinations thereof that are important in the establishment of infection.


Genetics ◽  
2021 ◽  
Vol 217 (1) ◽  
Author(s):  
Chia-En Tsai ◽  
Fang-Jung Yang ◽  
Ching-Han Lee ◽  
Yen-Ping Hsueh ◽  
Cheng-Ju Kuo ◽  
...  

Abstract Infection with antibiotic-resistant bacteria is an emerging life-threatening issue worldwide. Enterohemorrhagic Escherichia coli O157: H7 (EHEC) causes hemorrhagic colitis and hemolytic uremic syndrome via contaminated food. Treatment of EHEC infection with antibiotics is contraindicated because of the risk of worsening the syndrome through the secreted toxins. Identifying the host factors involved in bacterial infection provides information about how to combat this pathogen. In our previous study, we showed that EHEC colonizes in the intestine of Caenorhabditis elegans. However, the host factors involved in EHEC colonization remain elusive. Thus, in this study, we aimed to identify the host factors involved in EHEC colonization. We conducted forward genetic screens to isolate mutants that enhanced EHEC colonization and named this phenotype enhanced intestinal colonization (Inc). Intriguingly, four mutants with the Inc phenotype showed significantly increased EHEC-resistant survival, which contrasts with our current knowledge. Genetic mapping and whole-genome sequencing (WGS) revealed that these mutants have loss-of-function mutations in unc-89. Furthermore, we showed that the tolerance of unc-89(wf132) to EHEC relied on HLH-30/TFEB activation. These findings suggest that hlh-30 plays a key role in pathogen tolerance in C. elegans.


2021 ◽  
Vol 9 (9) ◽  
pp. 1823
Author(s):  
Maria Beatriz de Sousa de Sousa Figueiredo ◽  
Elizabeth Pradel ◽  
Fanny George ◽  
Séverine Mahieux ◽  
Isabelle Houcke ◽  
...  

The adherent-invasive Escherichia coli (AIEC) pathotype has been implicated in the pathogenesis of inflammatory bowel diseases in general and in Crohn’s disease (CD) in particular. AIEC strains are primarily characterized by their ability to adhere to and invade intestinal epithelial cells. However, the genetic and phenotypic features of AIEC isolates vary greatly as a function of the strain’s clonality, host factors, and the gut microenvironment. It is thus essential to identify the determinants of AIEC pathogenicity and understand their role in intestinal epithelial barrier dysfunction and inflammation. We reasoned that soil nematode Caenorhabditis elegans (a simple but powerful model of host-bacterium interactions) could be used to study the virulence of AIEC vs. non- AIEC E. coli strains. Indeed, we found that the colonization of C. elegans (strain N2) by E. coli impacted survival in a strain-specific manner. Moreover, the AIEC strains’ ability to invade cells in vitro was linked to the median lifespan in C. elegans (strain PX627). However, neither the E. coli intrinsic invasiveness (i.e., the fact for an individual strain to be characterized as invasive or not) nor AIEC’s virulence levels (i.e., the intensity of invasion, established in % from the infectious inoculum) in intestinal epithelial cells was correlated with C. elegans’ lifespan in the killing assay. Nevertheless, AIEC longevity of C. elegans might be a relevant model for screening anti-adhesion drugs and anti-invasive probiotics.


2019 ◽  
Vol 10 (1) ◽  
pp. 189-198 ◽  
Author(s):  
Isaiah A. A. Neve ◽  
Jessica N. Sowa ◽  
Chih-Chun J. Lin ◽  
Priya Sivaramakrishnan ◽  
Christophe Herman ◽  
...  

The relationship of genotypes to phenotypes can be modified by environmental inputs. Such crucial environmental inputs include metabolic cues derived from microbes living together with animals. Thus, the analysis of genetic effects on animals’ physiology can be confounded by variations in the metabolic profile of microbes. Caenorhabditis elegans exposed to distinct bacterial strains and species exhibit phenotypes different at cellular, developmental, and behavioral levels. Here we reported metabolomic profiles of three Escherichia coli strains, B strain OP50, K-12 strain MG1655, and B-K-12 hybrid strain HB101, as well as different mitochondrial and fat storage phenotypes of C. elegans exposed to MG1655 and HB101 vs. OP50. We found that these metabolic phenotypes of C. elegans are not correlated with overall metabolic patterning of bacterial strains, but their specific metabolites. In particular, the fat storage phenotype is traced to the betaine level in different bacterial strains. HT115 is another K-12 E. coli strain that is commonly utilized to elicit an RNA interference response, and we showed that C. elegans exposed to OP50 and HT115 exhibit differences in mitochondrial morphology and fat storage levels. We thus generated an RNA interference competent OP50 (iOP50) strain that can robustly and consistently knockdown endogenous C. elegans genes in different tissues. Together, these studies suggest the importance of specific bacterial metabolites in regulating the host’s physiology and provide a tool to prevent confounding effects when analyzing genotype-phenotype interactions under different bacterial backgrounds.


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