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Modeling Host-Microbiome Interactions in Caenorhabditis elegans

TEKLU K. GERBABA
TEKLU K. GERBABA
, 
LUKE GREEN-HARRISON
LUKE GREEN-HARRISON
 e 
ANDRE G. BURET
ANDRE G. BURET
   | 26 set 2018
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Pubblicato online: 26 set 2018
Pagine: 348 - 356
Ricevuto: 01 mar 2017
DOI: https://doi.org/10.21307/jofnem-2017-082
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© 2017 TEKLU K. GERBABA et al., published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

FIG. 1.

Laboratory growth and maintenance of Caenorhabditis elegans for use in host–microbe interaction studies. Gravid adult worms are transferred to a nematode growth medium agar plate previously seeded with OP50 Escherichia coli, a standard food source for C. elegans. (1) The worms will reproduce and populate the plate. (2) Gravid adult worms from the plate can then be transferred to a new plate (3) continuing the cycle. When there are enough eggs and gravid adults on the plate, they can be collected, transferred to a tube, and treated with bleach, which dissolves the worms and kills bacteria, leaving only the bleach-resistant eggs. (4) The eggs are washed and allowed to hatch and arrest at the L1 developmental stage in S-basal buffer, creating an age-synchronized germ-free population. (5) L1 worms are then resuspended in S-basal complete media, fed OP50 E. coli, and allowed to develop over 2 to 3 d to L4/adult worms. (6) These worms are ready for host–microbe interaction studies (7) as in Gerbaba et al. (2015).
Laboratory growth and maintenance of Caenorhabditis elegans for use in host–microbe interaction studies. Gravid adult worms are transferred to a nematode growth medium agar plate previously seeded with OP50 Escherichia coli, a standard food source for C. elegans. (1) The worms will reproduce and populate the plate. (2) Gravid adult worms from the plate can then be transferred to a new plate (3) continuing the cycle. When there are enough eggs and gravid adults on the plate, they can be collected, transferred to a tube, and treated with bleach, which dissolves the worms and kills bacteria, leaving only the bleach-resistant eggs. (4) The eggs are washed and allowed to hatch and arrest at the L1 developmental stage in S-basal buffer, creating an age-synchronized germ-free population. (5) L1 worms are then resuspended in S-basal complete media, fed OP50 E. coli, and allowed to develop over 2 to 3 d to L4/adult worms. (6) These worms are ready for host–microbe interaction studies (7) as in Gerbaba et al. (2015).

FIG. 2.

Host–microbe interactions in Caenorhabditis elegans. This figure summarizes host–microbe interactions in C. elegans discussed in the present review. Bacteria metabolic signals, such as folate, vitamin B12, tryptophan, methionine, nitric oxide (NO), cyclic antimicrobial peptide (AMP), and amyloid protein, influence various biological processes including germ cell proliferation, development, longevity, and neurodegeneration in C. elegans. Expression of folate receptors (FOR1) in C. elegans is essential to the modulatory effects of bacterial folate on germ cell proliferation. The nuclear hormone receptor (NHR-23) is likely involved in regulating the molting cycle during larval development (MacNeil et al., 2013), but the link between the effects of Caenorhabditis aquaticus vitamin B12 on the acceleration of development and NHRs is not clear (Watson et al., 2014). The effects of Escherichia coli HB101 on worm development (speeding growth) are target of rapamycin (TOR) dependent (MacNeil et al., 2013). Escherichia coli HT115 tryptophan mediates detoxification responses in nhr-114 mutant worms. Microbes are important sources of dietary methionine in C. elegans, and interference with microbial methionine synthesis induces methionine restriction, which in turn extends lifespan (Cabreiro et al., 2013). Bacillus subtilis NO extends worm lifespan, which is dependent on DAF-16 and HSF-1 transcription factors (Gusarov et al., 2013; Donato et al., 2017). Several studies using C. elegans have illustrated how the host microbiome may protect against pathogens (shown in dark red). Pseudomonas mendocina, Lactobacillus acidophilus, and Lactobacillus casei protect against pathogenic infection in a PMK-1 (p38 MAPK) or β-catenin signaling (BAR1) dependent manner. Lactobacillus reuteri protects against enterotoxigenic E. coli (ETEC) possibly through induction of expression of AMP genes. Bacillus megaterium–mediated protection against Pseudomonas infection is linked to impaired egg laying, the potential host response pathways involved remain obscure. Various lactic acid bacteria (LAB) alter expression of obesity phenotype genes (in green). Bacterial metabolite effects in eliciting neurodegeneration (light blue) have also been studied in C. elegans, but the specific bacterial metabolites implicated in these effects require further identification. The effects of C. elegans-microbial interactions on longevity, development, and germ cell proliferation are shown in orange.
Host–microbe interactions in Caenorhabditis elegans. This figure summarizes host–microbe interactions in C. elegans discussed in the present review. Bacteria metabolic signals, such as folate, vitamin B12, tryptophan, methionine, nitric oxide (NO), cyclic antimicrobial peptide (AMP), and amyloid protein, influence various biological processes including germ cell proliferation, development, longevity, and neurodegeneration in C. elegans. Expression of folate receptors (FOR1) in C. elegans is essential to the modulatory effects of bacterial folate on germ cell proliferation. The nuclear hormone receptor (NHR-23) is likely involved in regulating the molting cycle during larval development (MacNeil et al., 2013), but the link between the effects of Caenorhabditis aquaticus vitamin B12 on the acceleration of development and NHRs is not clear (Watson et al., 2014). The effects of Escherichia coli HB101 on worm development (speeding growth) are target of rapamycin (TOR) dependent (MacNeil et al., 2013). Escherichia coli HT115 tryptophan mediates detoxification responses in nhr-114 mutant worms. Microbes are important sources of dietary methionine in C. elegans, and interference with microbial methionine synthesis induces methionine restriction, which in turn extends lifespan (Cabreiro et al., 2013). Bacillus subtilis NO extends worm lifespan, which is dependent on DAF-16 and HSF-1 transcription factors (Gusarov et al., 2013; Donato et al., 2017). Several studies using C. elegans have illustrated how the host microbiome may protect against pathogens (shown in dark red). Pseudomonas mendocina, Lactobacillus acidophilus, and Lactobacillus casei protect against pathogenic infection in a PMK-1 (p38 MAPK) or β-catenin signaling (BAR1) dependent manner. Lactobacillus reuteri protects against enterotoxigenic E. coli (ETEC) possibly through induction of expression of AMP genes. Bacillus megaterium–mediated protection against Pseudomonas infection is linked to impaired egg laying, the potential host response pathways involved remain obscure. Various lactic acid bacteria (LAB) alter expression of obesity phenotype genes (in green). Bacterial metabolite effects in eliciting neurodegeneration (light blue) have also been studied in C. elegans, but the specific bacterial metabolites implicated in these effects require further identification. The effects of C. elegans-microbial interactions on longevity, development, and germ cell proliferation are shown in orange.
eISSN:
2640-396X
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