title: Selenite enhances immune response against Pseudomonas aeruginosa PA14 via SKN-1 in Caenorhabditis elegans.
abstract: BACKGROUND
  Selenium (Se) is an important nutrient that carries out many biological processes including maintaining optimal immune function. Here, inorganic selenite (Se(IV)) was evaluated for its pathogen resistance and potential-associated factors in Caenorhabditis elegans. The immune effects of Se(IV) were investigated by examining the responses of C. elegans to Pseudomonas aerugonisa PA14 strain.
  
  
  RESULTS
  Se(IV)-treated C. elegans showed increased survival under PA14 infection compared with untreated controls. The significant pathogen resistance of Se(IV) on C. elegans might not be attributed to the effects of Se(IV) on PA14 as Se(IV) showed no effect on bacterial quorum-sensing and virulence factors of PA14. This study showed that Se(IV) enhanced the expression of a gene pivotal for the innate immunity in C. elegans. The study found that the pathogen-resistant phenotypes contributed by Se(IV) was absent from the skn-1 mutant worms. Moreover, Se(IV) influenced the subcellular distribution of SKN-1/Nrf in C. elegans upon PA14 infection. Furthermore, Se(IV) increased mRNA levels of SKN-1 target genes (gst-4 and gcs-1).
  
  
  CONCLUSIONS
  This study found evidence of Se(IV) protecting C. elegans against P. aeruginosa PA14 infection by exerting effects on the innate immunity of C. elegans that is likely mediated via regulation of a SKN-1-dependent signaling pathway.
authors.affiliation: Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei, Taiwan.
authors.forename: Wen-Hsuan
authors.initials: WH
authors.lastname: Li
authors.affiliation: Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei, Taiwan.
authors.forename: Chun-Han
authors.initials: CH
authors.lastname: Chang
authors.affiliation: Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei, Taiwan.
authors.forename: Chi-Wei
authors.initials: CW
authors.lastname: Huang
authors.affiliation: Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei, Taiwan.
authors.forename: Chia-Cheng
authors.initials: CC
authors.lastname: Wei
authors.affiliation: Department of Bioenvironmental Systems Engineering, National Taiwan University, Taipei, Taiwan.
authors.forename: Vivian Hsiu-Chuan
authors.initials: VH
authors.lastname: Liao
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D018441:Biofilms; D017173:Caenorhabditis elegans / Q000187:drug effects* / Q000235:genetics / Q000276:immunology* / Q000382:microbiology; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000276:immunology* / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D005721:Glutamate-Cysteine Ligase / Q000235:genetics; D005982:Glutathione Transferase / Q000235:genetics; D011550:Pseudomonas aeruginosa / Q000187:drug effects / Q000235:genetics / Q000472:pathogenicity*; D053038:Quorum Sensing; D020887:Selenious Acid / Q000276:immunology / Q000494:pharmacology*; D014157:Transcription Factors / Q000276:immunology* / Q000378:metabolism; D037521:Virulence Factors / Q000235:genetics
chemical_list: D029742:Caenorhabditis elegans Proteins; D004268:DNA-Binding Proteins; D014157:Transcription Factors; D037521:Virulence Factors; C073702:skn-1 protein, C elegans; D005982:Glutathione Transferase; D005721:Glutamate-Cysteine Ligase; D020887:Selenious Acid