Recovery from an acute infection in C. elegans requires the GATA transcription factor ELT-2.
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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.
Caenorhabditis elegans Proteins
Disease Models, Animal
GATA Transcription Factors
Published Version (Please cite this version)10.1371/journal.pgen.1004609
Publication InfoHead, B; & Aballay, A (2014). Recovery from an acute infection in C. elegans requires the GATA transcription factor ELT-2. PLoS Genet, 10(10). pp. e1004609. 10.1371/journal.pgen.1004609. Retrieved from https://hdl.handle.net/10161/9200.
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Adjunct Professor in the Department of Molecular Genetics and Microbiology
Our laboratory uses genetic and functional genomic methodologies to study the genetic basis of innate immunity using C. elegans and mammalian systems. Recent studies from our laboratory highlight the importance of the nervous system in the regulation of innate immune responses. Using a genetic approach we were able to demonstrate that specific neurons can regulate innate immunit