Interkingdom signaling between pathogenic bacteria and Caenorhabditis elegans.
Investigators have recently turned to the soil nematode Caenorhabditis elegans as a small animal infection model to study infectious disease. To extrapolate findings concerning bacterial pathogenesis from non-mammals to mammals, virulence factors should be conserved in function, independent of the infection model. Emerging from these studies is the observation that bacterial virulence regulatory networks function in a conserved manner across multiple hosts, including nematodes, mice and plants. Several regulatory networks have been implicated in nematode innate immune function and are being exploited in the C. elegans infection model to develop novel chemical therapies against bacterial pathogens.
Mellies
Jay L
JL
Department of Biology, Reed College, Portland, OR 97202, USA. jay.mellies@reed.edu
Lawrence-Pine
Emily R
ER
D000818:Animals; D001419:Bacteria / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity*; D001424:Bacterial Infections / Q000382:microbiology*; D017173:Caenorhabditis elegans / Q000235:genetics / Q000276:immunology / Q000382:microbiology*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D055808:Drug Discovery; D053263:Gene Regulatory Networks; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D053038:Quorum Sensing; D012808:Sigma Factor / Q000235:genetics / Q000378:metabolism; D014774:Virulence
D029742:Caenorhabditis elegans Proteins; D012808:Sigma Factor