Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2008 Nov-Dec;1(4-5):205-8.
doi: 10.1242/dmm.000265.

Studying host-pathogen interactions and innate immunity in Caenorhabditis elegans

Affiliations

Studying host-pathogen interactions and innate immunity in Caenorhabditis elegans

Dennis Kim. Dis Model Mech. 2008 Nov-Dec.

Abstract

The genetic analysis of mechanisms of pathogen resistance in the nematode Caenorhabditis elegans has revealed a role for evolutionarily conserved signaling pathways that are required for innate immunity in a wide range of organisms, from worms to mammals. C. elegans represents one of the more simple host organisms in which mechanisms of host defense can be dissected, and the use of C. elegans presents the researcher with a wide array of genetic and genomic tools to probe the host-pathogen interface. The study of host defense mechanisms in C. elegans continues to provide an ancient evolutionary perspective on innate immunity, which may generate insights into the conserved processes in phylogenetically diverse host organisms, including humans.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Different modes of infection of C. elegans elicit immune responses. Three distinct modes of infection of C. elegans have been described that elicit conserved innate immune signaling pathways. (A) Intestinal infection with a wide range of pathogens involves proliferation of bacteria in the intestinal lumen. (B) The nematophagous fungus Drechmeria initiates infection by attachment to the cuticle with subsequent penetration of the epidermis. (C) The attachment of M. nematophilum to the tail region of C. elegans and subsequent rectal invasion induces a protective swelling response at the site of infection.

Similar articles

Cited by

References

    1. Aballay A., Yorgey P., Ausubel F. M. (2000). Salmonella typhimurium proliferates and establishes a persistent infection in the intestine of Caenorhabditis elegans. Curr. Biol. 10, 1539–1542 - PubMed
    1. Aballay A., Drenkard E., Hilbun L. R., Ausubel F. M. (2003). Caenorhabditis elegans innate immune response triggered by Salmonella enterica requires intact LPS and is mediated by a MAPK signaling pathway. Curr. Biol. 13, 47–52 - PubMed
    1. Akira S., Uematsu S., Takeuchi O. (2006). Pathogen recognition and innate immunity. Cell 124, 783–801 - PubMed
    1. Carty M., Goodbody R., Schroder M., Stack J., Moynagh P. N., Bowie A. G. (2006). The human adaptor SARM negatively regulates adaptor protein TRIF-dependent Toll-like receptor signaling. Nat. Immunol. 7, 1074–1081 - PubMed
    1. Chavez V., Mohri-Shiomi A., Maadani A., Vega L. A., Garsin D. A. (2007). Oxidative stress enzymes are required for DAF-16-mediated immunity due to generation of reactive oxygen species by Caenorhabditis elegans. Genetics 176, 1567–1577 - PMC - PubMed

MeSH terms