scholarly journals From pathogen to commensal to probiotic: modification of Microbacterium nematophilum-C. elegans interaction during chronic infection by the absence of host insulin signalling

2020 ◽  
Author(s):  
Maria Gravato-Nobre ◽  
Jonathan Hodgkin ◽  
Petros Ligoxygakis
Keyword(s):  
Chronic Infection ◽  
Insulin Signalling ◽  
Avirulent Strain ◽  
Opportunistic Pathogens ◽  
E Coli ◽  
C Elegans ◽  
Intestinal Infections ◽  
Age Dependent ◽  
Immune Defences ◽  
Nematode Worm

ABSTRACTThe nematode worm Caenorhabditis elegans depends on microbes in decaying vegetation as its food source. To survive in an environment rich in opportunistic pathogens, C. elegans has evolved an epithelial defence system where surface-exposed tissues such as epidermis, pharynx, intestine, vulva and hindgut have the capacity of eliciting appropriate immune defences to acute gut infection. However, it is unclear how the worm responds to chronic intestinal infections. To this end, we have surveyed C. elegans mutants that are involved in inflammation, immunity and longevity to find their phenotypes during chronic infection. Worms that grew in a monoculture of the natural pathogen Microbacterium nematophilum (CBX102 strain) had a reduced lifespan and health span. This was independent of intestinal colonisation as both CBX102 and the derived avirulent strain UV336 were early persistent colonisers. In contrast, long-lived daf-2 mutants were resistant to chronic infection, showing reduced colonisation and a higher age-dependent vigour. In fact, UV336 acted as a probiotic in daf-2, showing a lifespan extension beyond OP50, the E. coli strain used for laboratory C. elegans culture. Longevity and vigour of daf-2 mutants growing on CBX102 was dependent on the FOXO orthologue DAF-16. Since the DAF-2/DAF-16 axis is present in most metazoans this suggests an evolutionary conserved host mechanism to modify a pathogen to a commensal.

scholarly journals From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling

Biology Open ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. bio053504
Author(s):  
Maria Gravato-Nobre ◽  
Jonathan Hodgkin ◽  
Petros Ligoxygakis
Keyword(s):  
Caenorhabditis Elegans ◽  
Chronic Infection ◽  
Insulin Signalling ◽  
Avirulent Strain ◽  
Opportunistic Pathogens ◽  
Host Genotype ◽  
C Elegans ◽  
Intestinal Infections ◽  
Immune Defences ◽  
Nematode Worm

ABSTRACTThe nematode worm Caenorhabditis elegans depends on microbes in decaying vegetation as its food source. To survive in an environment rich in opportunistic pathogens, C. elegans has evolved an epithelial defence system where surface-exposed tissues such as epidermis, pharynx, intestine, vulva and hindgut have the capacity of eliciting appropriate immune defences to acute gut infection. However, it is unclear how the worm responds to chronic intestinal infections. To this end, we have surveyed C. elegans mutants that are involved in inflammation, immunity and longevity to find their phenotypes during chronic infection. Worms that grew in a monoculture of the natural pathogen Microbacterium nematophilum (CBX102 strain) had a reduced lifespan and vigour. This was independent of intestinal colonisation as both CBX102 and the derived avirulent strain UV336 were early persistent colonisers. In contrast, the long-lived daf-2 mutant was resistant to chronic infection, showing reduced colonisation and higher vigour. In fact, UV336 interaction with daf-2 resulted in a host lifespan extension beyond OP50, the Escherichia coli strain used for laboratory C. elegans culture. Longevity and vigour of daf-2 mutants growing on CBX102 was dependent on the FOXO orthologue DAF-16. Our results indicate that the interaction between host genotype and strain-specific bacteria determines longevity and health for C. elegans.

scholarly journals Toxin production and haemagglutination in strains ofEscherichia colifrom diarrhoea in Brescia, Italy

1985 ◽  
Vol 95 (2) ◽  
pp. 353-361 ◽  
Author(s):  
R. Bisicchia ◽  
R. Ciammarughi ◽  
A. Caprioli ◽  
V. Falbo ◽  
F. M. Ruggeri
Keyword(s):  
Escherichia Coli ◽  
Cell Cultures ◽  
Healthy Subjects ◽  
Strong Association ◽  
Toxin Production ◽  
Opportunistic Pathogens ◽  
E Coli ◽  
Intestinal Infections ◽  
Different Strains

SUMMARYTwo hundred and ninety-nine different strains ofEscherichia coli, isolated from 172 patients with diarrhoea and 113 healthy subjects, were examined for enterotoxin, cytotoxin and haemolysin (Hly) production and for mannose-resistant haemagglutination (MRHA) and invasive properties. Three strains proved enterotoxigenic, none enteroinvasive; cytotoxin and Hly production was shown in 25 strains from patients and in 3 from controls. Ten strains produced the cytotoxic necrotizing factor (CNF), 6 released other factors which kill cell cultures. Hly production was shown in 21 strains, 9 of which were also positive for CNF. MRHA was detected in 26% of strains from diarrhoca compared with 14% of strains from healthy people. A strong association between toxin production and MRHA was demonstrated. Serotyping results showed that the strains exhibiting virulence traits mostly belonged to serogroups commonly involved in extra-intestinal infections. The possible role of strains ofE. colishowing one or more virulence factors as opportunistic pathogens in diarrhoeal diseases is discussed.

scholarly journals Folic acid preventsC. elegansfolate deficiency indirectly via bacterial uptake of a breakdown product: a route that can also increase bacterial toxicity and ageing

2017 ◽  
Author(s):  
Claire Maynard ◽  
Ian Cummins ◽  
Jacalyn Green ◽  
David Weinkove
Keyword(s):  
Folic Acid ◽  
Folate Deficiency ◽  
Breakdown Product ◽  
E Coli ◽  
C Elegans ◽  
Bacterial Uptake ◽  
Major Route ◽  
Bacterial Toxicity ◽  
Health Complications ◽  
Nematode Worm

AbstractSupplementation with the synthetic oxidised folate, folic acid is used to prevent neural tube defects and other symptoms of folate deficiency. However, several unanswered questions remain over folic acid efficacy, safety and interactions with gut microbes. Prevention of a development defect caused by folate deficiency in the nematode wormCaenorhabditis elegansrequires > 10 fold higher concentrations of folic acid compared to folinic acid, a reduced folate. Here we show that the major route for folic acid to restore normal development is indirect via theEscherichia coliused to feedC. elegans.This route occurs mainly via theE. colitransporter AbgT, which takes up the folic acid breakdown product para-aminobenzoate-glutamate (PABA-glu). We found that folic acid preparations, including a commercial supplement, contain 0.3- 4.0 % of this breakdown product. Previously, we have shown that inhibiting bacterial folate synthesis increasesC. eleganslifespan by removing a life-shortening bacterial activity. Here, we show that folic acid restores bacterial folate synthesis and reverses this lifespan increase. It is still to be determined whether this bacterial route increases host folate levels in humans and if there are situations where increased bacterial folate synthesis has negative health complications.

scholarly journals Lactobacilli in a clade ameliorate age-dependent decline of thermotaxis behavior in Caenorhabditis elegans

2020 ◽  
Author(s):  
Satoshi Higurashi ◽  
Sachio Tsukada ◽  
Shunji Nakano ◽  
Ikue Mori ◽  
Kentaro Noma
Keyword(s):  
Caenorhabditis Elegans ◽  
Brain Aging ◽  
Genetic Manipulation ◽  
Aging Research ◽  
E Coli ◽  
C Elegans ◽  
Powerful Approach ◽  
Age Dependent ◽  
Long Time ◽  
Standard Laboratory Diet

AbstractDiet is proposed to affect brain aging. However, the causality and mechanism of dietary effects on brain aging are still unclear due to the long time scales of aging. The nematode Caenorhabditis elegans (C. elegans) has led aging research because of its short lifespan and easy genetic manipulation. When fed the standard laboratory diet, Escherichia coli (E. coli), C. elegans experiences an age-dependent decline in temperature-food associative learning, called thermotaxis. To address if diet ameliorates this decline, we screened 35 different lactic acid bacteria as alternative diets. We found that Lactobacilli in a clade enriched with heterofermentative bacteria ameliorated age-dependent decline. On the other hand, homofermentative Lactobacillus species did not show this beneficial effect. Lactobacilli affected the thermotaxis of aged animals through DAF-16, an ortholog of mammalian FOXO transcription factor, while the effect on the thermotaxis was independent of the lifespan and locomotion. Our results demonstrate that diet can impact brain aging without changing the lifespan and that bacterial screen using C. elegans is a powerful approach to investigate age-dependent behavioral decline.

scholarly journals Model super-organisms: Can the biochemical genetics of E. coli help us understand aging?

2015 ◽  
Vol 37 (4) ◽  
pp. 12-15
Author(s):  
David Weinkove
Keyword(s):  
Biosynthetic Pathway ◽  
Model Organism ◽  
Toxin Production ◽  
Enzyme Function ◽  
Nutrient Media ◽  
E Coli ◽  
C Elegans ◽  
Biochemical Pathways ◽  
Nematode Worm ◽  
Worm Caenorhabditis Elegans

Escherichia coli is a powerful model organism to help us understand biochemical pathways and enzyme function. In E. coli, biosynthetic pathway mutants are conditionally viable depending on the composition of the nutrient media. Genetic analysis allows enzyme function to be linked to gene sequences. E. coli is used in the lab as a food source for the nematode worm Caenorhabditis elegans, a model organism for the understanding of basic animal biology. Recent work has shown that specific biosynthetic pathways in E. coli can influence C. elegans aging. Careful experimentation is needed to determine whether E. coli biochemistry influences aging by altering C. elegans nutrition or through changes to bacterial functions, such as toxin production. Understanding these interactions in the C. elegans–E. coli model “super-organism” will inform studies of how bacteria of the human microbiota interact with the host.

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

The Effect of Mianserin on Lifespan of Caenorhabditis elegans is Abolished by Glucose

2021 ◽  
Vol 13 ◽  
Author(s):  
Abdullah Almotayri ◽  
Jency Thomas ◽  
Mihiri Munasinghe ◽  
Markandeya Jois
Keyword(s):  
Caenorhabditis Elegans ◽  
Scaffolding Protein ◽  
Lifespan Extension ◽  
Wild Type ◽  
E Coli ◽  
C Elegans ◽  
Risk Of Death ◽  
Increased Risk ◽  
Antidepressant Use ◽  
Extension Effect

Background: The antidepressant mianserin has been shown to extend the lifespan of Caenorhabditis elegans (C. elegans), a well-established model organism used in aging research. The extension of lifespan in C. elegans was shown to be dependent on increased expression of the scaffolding protein (ANK3/unc-44). In contrast, antidepressant use in humans is associated with an increased risk of death. The C. elegans in the laboratory are fed Escherichia coli (E. coli), a diet high in protein and low in carbohydrate, whereas a typical human diet is high in carbohydrates. We hypothesized that dietary carbohydrates might mitigate the lifespan-extension effect of mianserin. Objective: To investigate the effect of glucose added to the diet of C. elegans on the lifespan-extension effect of mianserin. Methods: Wild-type Bristol N2 and ANK3/unc-44 inactivating mutants were cultured on agar plates containing nematode growth medium and fed E. coli. Treatment groups included (C) control, (M50) 50 μM mianserin, (G) 73 mM glucose, and (M50G) 50 μM mianserin and 73 mM glucose. Lifespan was determined by monitoring the worms until they died. Statistical analysis was performed using the Kaplan-Meier version of the log-rank test. Results: Mianserin treatment resulted in a 12% increase in lifespan (P<0.05) of wild-type Bristol N2 worms but reduced lifespan by 6% in ANK3/unc-44 mutants, consistent with previous research. The addition of glucose to the diet reduced the lifespan of both strains of worms and abolished the lifespan-extension by mianserin. Conclusion: The addition of glucose to the diet of C. elegans abolishes the lifespan-extension effects of mianserin.

scholarly journals Iron Acquisition of Urinary Tract Infection Escherichia coli Involves Pathogenicity in Caenorhabditis elegans

2021 ◽  
Vol 9 (2) ◽  
pp. 310
Author(s):  
Masayuki Hashimoto ◽  
Yi-Fen Ma ◽  
Sin-Tian Wang ◽  
Chang-Shi Chen ◽  
Ching-Hao Teng
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Caenorhabditis Elegans ◽  
Large Scale ◽  
Iron Acquisition ◽  
Infection Model ◽  
High Throughput Analysis ◽  
E Coli ◽  
C Elegans ◽  
Tract Infections

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.

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