External induction of heat shock stimulates the immune response and longevity of Caenorhabditis elegans towards pathogen exposure

Innate Immun. 2016 Aug;22(6):466-78. doi: 10.1177/1753425916654557. Epub 2016 Jun 17.

Abstract

Heat shock proteins (HSPs) are highly chaperonic molecules that give immediate response during any stress, tissue damage or bacterial infections. In the present study, the role of HSPs upon bacterial encounter is studied by applying external heat induction to live Caenorhabditis elegans Heat shock was observed to increase the life span of wild type C. elegans upon pathogenic encounter, indicating a role of HSPs in bacterial infection and immunity. Similar increase in resistance towards pathogenesis observed in long-lived C. elegans daf-2 mutants and the increase in the lifespan indicated a role for the insulin/IGF-1 signaling (IIS) pathway in HSP-mediated pathogenic resistance. The microscopic observation of C. elegans after external heat induction and sequential exposure of pathogens indicated reduction of egg viability. Results of Real-time PCR and immunoblotting analysis of candidate genes revealed that heat shock and IIS pathways collaborate in the observed pathogenic resistance and further suggested SGK-1 to be the possible factor linking both these pathways. In addition, survival assays carried out using mutants equips us with supporting evidence that HSP and HSF-1 are necessary for the accelerated lifespan of C. elegans Our findings thus confirm that crosstalk between HSPs and SGK-1 influences C. elegans longevity.

Keywords: C. elegans; heat shock factor; heat shock proteins; insulin signaling pathway; longevity; pathogen resistance.

MeSH terms

  • Animals
  • Bacterial Infections / genetics
  • Bacterial Infections / immunology*
  • Caenorhabditis elegans / immunology*
  • Caenorhabditis elegans Proteins / genetics
  • Caenorhabditis elegans Proteins / metabolism*
  • Cells, Cultured
  • Environmental Exposure / adverse effects
  • Heat-Shock Proteins / metabolism*
  • Hot Temperature / adverse effects
  • Immunity, Innate
  • Insulin / metabolism
  • Insulin-Like Growth Factor I / metabolism
  • Models, Animal
  • Mutation / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Receptor, Insulin / genetics
  • Receptor, Insulin / metabolism*
  • Signal Transduction / genetics

Substances

  • Caenorhabditis elegans Proteins
  • Heat-Shock Proteins
  • Insulin
  • Insulin-Like Growth Factor I
  • DAF-2 protein, C elegans
  • Receptor, Insulin
  • Protein Serine-Threonine Kinases
  • Sgk-1 protein, C elegans