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Recovery from an acute infection in C. elegans requires the GATA transcription factor ELT-2.

dc.contributor.author Head, Brian
dc.contributor.author Aballay, Alejandro
dc.coverage.spatial United States
dc.date.accessioned 2014-10-28T13:21:41Z
dc.date.issued 2014-10
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/25340560
dc.identifier PGENETICS-D-14-00123
dc.identifier.uri https://hdl.handle.net/10161/9200
dc.description.abstract The mechanisms involved in the recognition of microbial pathogens and activation of the immune system have been extensively studied. However, the mechanisms involved in the recovery phase of an infection are incompletely characterized at both the cellular and physiological levels. Here, we establish a Caenorhabditis elegans-Salmonella enterica model of acute infection and antibiotic treatment for studying biological changes during the resolution phase of an infection. Using whole genome expression profiles of acutely infected animals, we found that genes that are markers of innate immunity are down-regulated upon recovery, while genes involved in xenobiotic detoxification, redox regulation, and cellular homeostasis are up-regulated. In silico analyses demonstrated that genes altered during recovery from infection were transcriptionally regulated by conserved transcription factors, including GATA/ELT-2, FOXO/DAF-16, and Nrf/SKN-1. Finally, we found that recovery from an acute bacterial infection is dependent on ELT-2 activity.
dc.language eng
dc.publisher Public Library of Science (PLoS)
dc.relation.ispartof PLoS Genet
dc.relation.isversionof 10.1371/journal.pgen.1004609
dc.subject Animals
dc.subject Caenorhabditis elegans
dc.subject Caenorhabditis elegans Proteins
dc.subject Computer Simulation
dc.subject Disease Models, Animal
dc.subject GATA Transcription Factors
dc.subject Immunity, Innate
dc.subject Inactivation, Metabolic
dc.subject Infection
dc.subject Salmonella enterica
dc.subject Transcriptome
dc.subject Wound Healing
dc.title Recovery from an acute infection in C. elegans requires the GATA transcription factor ELT-2.
dc.type Journal article
duke.contributor.id Aballay, Alejandro|0296653
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/25340560
pubs.begin-page e1004609
pubs.issue 10
pubs.organisational-group Basic Science Departments
pubs.organisational-group Duke
pubs.organisational-group Duke Institute for Brain Sciences
pubs.organisational-group Institutes and Provost's Academic Units
pubs.organisational-group Molecular Genetics and Microbiology
pubs.organisational-group School of Medicine
pubs.organisational-group University Institutes and Centers
pubs.publication-status Published online
pubs.volume 10
dc.identifier.eissn 1553-7404


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