title: The Conserved G-Protein Coupled Receptor FSHR-1 Regulates Protective Host Responses to Infection and Oxidative Stress.
abstract: The innate immune system's ability to sense an infection is critical so that it can rapidly respond if pathogenic microorganisms threaten the host, but otherwise maintain a quiescent baseline state to avoid causing damage to the host or to commensal microorganisms. One important mechanism for discriminating between pathogenic and non-pathogenic bacteria is the recognition of cellular damage caused by a pathogen during the course of infection. In Caenorhabditis elegans, the conserved G-protein coupled receptor FSHR-1 is an important constituent of the innate immune response. FSHR-1 activates the expression of antimicrobial infection response genes in infected worms and delays accumulation of the ingested pathogen Pseudomonas aeruginosa. FSHR-1 is central not only to the worm's survival of infection by multiple pathogens, but also to the worm's survival of xenobiotic cadmium and oxidative stresses. Infected worms produce reactive oxygen species to fight off the pathogens; FSHR-1 is required at the site of infection for the expression of detoxifying genes that protect the host from collateral damage caused by this defense response. Finally, the FSHR-1 pathway is important for the ability of worms to discriminate pathogenic from benign bacteria and subsequently initiate an aversive learning program that promotes selective pathogen avoidance.
authors.affiliation: Department of Biology, Gettysburg College, Gettysburg, Pennsylvania, United States of America.
authors.forename: Elizabeth V
authors.initials: EV
authors.lastname: Miller
authors.affiliation: Department of Biology, Gettysburg College, Gettysburg, Pennsylvania, United States of America.
authors.forename: Leah N
authors.initials: LN
authors.lastname: Grandi
authors.affiliation: Department of Biology, Gettysburg College, Gettysburg, Pennsylvania, United States of America.
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Giannini
authors.affiliation: Department of Biology, Gettysburg College, Gettysburg, Pennsylvania, United States of America.
authors.forename: Joseph D
authors.initials: JD
authors.lastname: Robinson
authors.affiliation: Department of Biology, Gettysburg College, Gettysburg, Pennsylvania, United States of America.
authors.forename: Jennifer R
authors.initials: JR
authors.lastname: Powell
mesh_terms: D000818:Animals; D060467:Disease Resistance / Q000235:genetics / Q000276:immunology; D005786:Gene Expression Regulation; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000276:immunology; D007239:Infections / Q000235:genetics* / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000401:mortality; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology; D019216:Metals, Heavy / Q000378:metabolism; D009154:Mutation; D018384:Oxidative Stress / Q000235:genetics / Q000276:immunology; D011962:Receptors, FSH / Q000235:genetics* / Q000378:metabolism*; D013312:Stress, Physiological / Q000235:genetics / Q000276:immunology
chemical_list: D019216:Metals, Heavy; D011962:Receptors, FSH