A two-gene balance regulates Salmonella typhimurium tolerance in the nematode Caenorhabditis elegans

Lysozymes are antimicrobial enzymes that perform a critical role in resisting infection in a wide-range of eukaryotes. However, using the nematode Caenorhabditis elegans as a model host we now demonstrate that deletion of the protist type lysozyme LYS-7 renders animals susceptible to killing by the...

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Published in:PloS one 2011-03, Vol.6 (3), p.e16839
Main Authors: Marsh, Elizabeth K, van den Berg, Maaike C W, May, Robin C
Format: Article
Language:English
Subjects:
Adaptation, Physiological - genetics
Analysis
Animals
Antimicrobial agents
Autoimmune diseases
Bacteria
Bacterial genetics
Biochemistry
Biology
Caenorhabditis
Caenorhabditis elegans
Caenorhabditis elegans - enzymology
Caenorhabditis elegans - genetics
Caenorhabditis elegans - microbiology
Caenorhabditis elegans Proteins - genetics
Cryptococcosis - genetics
Cryptococcosis - microbiology
Cryptococcus neoformans
Cryptococcus neoformans - physiology
Cytokines
Dosage Compensation, Genetic
Drosophila
Drosophila melanogaster
Enzymes
Eukaryotes
Fungal infections
Gene expression
Genes, Helminth - genetics
Genetic aspects
Genetic engineering
Humans
Immune response
Immunological tolerance
Immunology
Insects
Kinases
Listeria
Lysozyme
Muramidase - genetics
Mutation - genetics
Nematodes
Phenotype
Protein-tyrosine kinase
Proto-Oncogene Proteins c-abl - genetics
Roundworms
Salmonella
Salmonella Infections, Animal - genetics
Salmonella Infections, Animal - microbiology
Salmonella typhimurium
Salmonella typhimurium - physiology
Staphylococcus infections
Suppression, Genetic
Tyrosine
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van den Berg, Maaike C W
May, Robin C
description Lysozymes are antimicrobial enzymes that perform a critical role in resisting infection in a wide-range of eukaryotes. However, using the nematode Caenorhabditis elegans as a model host we now demonstrate that deletion of the protist type lysozyme LYS-7 renders animals susceptible to killing by the fatal fungal human pathogen Cryptococcus neoformans, but, remarkably, enhances tolerance to the enteric bacteria Salmonella Typhimurium. This trade-off in immunological susceptibility in C. elegans is further mediated by the reciprocal activity of lys-7 and the tyrosine kinase abl-1. Together this implies a greater complexity in C. elegans innate immune function than previously thought.
doi_str_mv 10.1371/journal.pone.0016839
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subjects Adaptation, Physiological - genetics
Analysis
Animals
Antimicrobial agents
Autoimmune diseases
Bacteria
Bacterial genetics
Biochemistry
Biology
Caenorhabditis
Caenorhabditis elegans
Caenorhabditis elegans - enzymology
Caenorhabditis elegans - genetics
Caenorhabditis elegans - microbiology
Caenorhabditis elegans Proteins - genetics
Cryptococcosis - genetics
Cryptococcosis - microbiology
Cryptococcus neoformans
Cryptococcus neoformans - physiology
Cytokines
Dosage Compensation, Genetic
Drosophila
Drosophila melanogaster
Enzymes
Eukaryotes
Fungal infections
Gene expression
Genes, Helminth - genetics
Genetic aspects
Genetic engineering
Humans
Immune response
Immunological tolerance
Immunology
Insects
Kinases
Listeria
Lysozyme
Muramidase - genetics
Mutation - genetics
Nematodes
Phenotype
Protein-tyrosine kinase
Proto-Oncogene Proteins c-abl - genetics
Roundworms
Salmonella
Salmonella Infections, Animal - genetics
Salmonella Infections, Animal - microbiology
Salmonella typhimurium
Salmonella typhimurium - physiology
Staphylococcus infections
Suppression, Genetic
Tyrosine
title A two-gene balance regulates Salmonella typhimurium tolerance in the nematode Caenorhabditis elegans
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