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

The 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 hin...

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Autores principales: Gravato-Nobre, Maria, Hodgkin, Jonathan, Ligoxygakis, Petros
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Company of Biologists Ltd 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7561485/
https://www.ncbi.nlm.nih.gov/pubmed/32580971
http://dx.doi.org/10.1242/bio.053504
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author Gravato-Nobre, Maria
Hodgkin, Jonathan
Ligoxygakis, Petros
author_facet Gravato-Nobre, Maria
Hodgkin, Jonathan
Ligoxygakis, Petros
author_sort Gravato-Nobre, Maria
collection PubMed
description The 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.
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spelling pubmed-75614852020-10-19 From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling Gravato-Nobre, Maria Hodgkin, Jonathan Ligoxygakis, Petros Biol Open Research Article The 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. The Company of Biologists Ltd 2020-10-07 /pmc/articles/PMC7561485/ /pubmed/32580971 http://dx.doi.org/10.1242/bio.053504 Text en © 2020. Published by The Company of Biologists Ltd http://creativecommons.org/licenses/by/4.0This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
spellingShingle Research Article
Gravato-Nobre, Maria
Hodgkin, Jonathan
Ligoxygakis, Petros
From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling
title From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling
title_full From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling
title_fullStr From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling
title_full_unstemmed From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling
title_short From pathogen to a commensal: modification of the Microbacterium nematophilum–Caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling
title_sort from pathogen to a commensal: modification of the microbacterium nematophilum–caenorhabditis elegans interaction during chronic infection by the absence of host insulin signalling
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7561485/
https://www.ncbi.nlm.nih.gov/pubmed/32580971
http://dx.doi.org/10.1242/bio.053504
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