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.





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Head, Brian, and Alejandro Aballay (2014). Recovery from an acute infection in C. elegans requires the GATA transcription factor ELT-2. PLoS Genet, 10(10). p. e1004609. 10.1371/journal.pgen.1004609 Retrieved from

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Alejandro Aballay

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 immunity. We are studying a number of signaling molecules that can be used by the nervous and immune system to communicate to each other. We infect the Caenorhabditis elegans model host with different human bacterial and fungal pathogens to understand host-pathogen interactions. We also use mammalian systems to study innate immunity and microbial pathogenesis.

Another line of investigation we are pursuing concerns the identification and characterization of receptors potentially involved in pathogen recognition and activation of immune responses. We have demonstrated that the only Toll-like receptor in C. elegans, TOL-1 is required to prevent the invasion of pharyngeal cells by the human pathogen Salmonella enterica. The study of candidate downstream components of the TOL-1 pathway indicate that TRF-1, but not IKB-1, may be required for the effects of TOL-1 in immunity and that there may be other downstream components that regulate TOL-1-mediated immunity in a redundant manner. We are also studying the immune function of the scavenger receptor CED-1 and a system of proteins involved in the unfolding protein response (UPR) that are required to prevent bacterial invasion of host cells.

In addition to pathogen recognition and activation of microbial killing pathways, another important aspect of innate immune response is fever. Fever is an ancient immune mechanism used by metazoans in response to microbial infections. In mammals, several studies have been conducted to understand the mechanism of fever elicitation and to develop antipyretic therapeutics. However, the mechanism by which increased temperature exerts its beneficial role remains unclear. We use C. elegans to study the mechanism by which increased temperatures activate the innate immune system.

We are also characterizing different C. elegans mutants that are either more resistant or more susceptible to
pathogens. Since several components of innate immunity are conserved among different organisms throughout evolution, understanding the basis of the immune response in C. elegans should provide new insight into some aspects of immunity in mammals.

Finally, we study the mechanisms by which bacterial virulence factors required for virulence in both nematodes and mammals target conserved innate immune pathways. We have demonstrated that S. enterica genes related to the type three secretion system (TTSS) are expressed in the C. elegans intestine and required for full virulence. We also showed that the S. enterica TTSS-exported effector protein SptP inhibits a conserved P38 MAPK signaling pathway. In addition to S. enterica, we also perform studies using a variety of human pathogens including Yersinia pestis, Pseudomonas aeruginosa, Staphylococcus aureus, and Cryptococcus neoformans.

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