title: Altered gene expression and possible immunodeficiency in cases of sudden infant death syndrome.
abstract: A large number of studies have tried to uncover a genetic predisposition for sudden infant death syndrome (SIDS), but there is still uncertainty concerning the pathogenesis of these deaths. The purpose of this study was to investigate mRNA gene expression in SIDS cases and controls, in order to uncover genes that are differentially expressed in the two groups.
  
  
  
  Tissue from brain, heart, and liver from 15 SIDS cases and 15 controls were included in the study, and mRNA expression was determined using the Illumina whole genome gene expression DASL HT assay.
  
  
  
  Seventeen genes showed significantly altered expression compared to controls, after correction for multiple testing. Three genes involved in the immune system were of particular interest, including the downregulation of MyD88 in tissue from SIDS brains, as well as the downregulation of the genes encoding CCL3 and UNC13 in the liver.
  
  
  
  These findings indicate that there is an altered expression of genes involved in the inflammatory process in a proportion of SIDS cases, which further strengthen the hypothesis that impaired immune response play a role in this syndrome.
authors.affiliation: Department of Pediatric Forensic Medicine, Norwegian Institute of Public Health, Oslo, Norway.
authors.forename: Linda
authors.identifier: 0000-0003-1642-2737
authors.initials: L
authors.lastname: Ferrante
authors.affiliation: Department of Pediatric Forensic Medicine, Norwegian Institute of Public Health, Oslo, Norway.
authors.forename: Torleiv O
authors.initials: TO
authors.lastname: Rognum
authors.affiliation: Department of Pediatric Forensic Medicine, Norwegian Institute of Public Health, Oslo, Norway.
authors.forename: Åshild
authors.initials: Å
authors.lastname: Vege
authors.affiliation: Bioinformatics Core Facility, Institute for Medical Informatics, Oslo University Hospital, Oslo, Norway.
authors.forename: Ståle
authors.initials: S
authors.lastname: Nygård
authors.affiliation: Department of Pediatric Forensic Medicine, Norwegian Institute of Public Health, Oslo, Norway.|Department of Pathology, Oslo University Hospital, Oslo, Norway.
authors.forename: Siri H
authors.initials: SH
authors.lastname: Opdal
mesh_terms: D016022:Case-Control Studies; D054405:Chemokine CCL3 / Q000235:genetics*; D002675:Child, Preschool; D005260:Female; D020869:Gene Expression Profiling; D020022:Genetic Predisposition to Disease; D006801:Humans; D007107:Immune System; D007153:Immunologic Deficiency Syndromes / Q000235:genetics*; D007223:Infant; D008099:Liver / Q000378:metabolism; D008297:Male; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics*; D009419:Nerve Tissue Proteins / Q000235:genetics*; D020411:Oligonucleotide Array Sequence Analysis; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction; D013211:Staphylococcus aureus; D013290:Streptococcal Infections; D013296:Streptococcus pneumoniae; D013398:Sudden Infant Death / Q000235:genetics*; D014018:Tissue Distribution
chemical_list: C515429:CCL3 protein, human; D054405:Chemokine CCL3; C507779:MYD88 protein, human; D053594:Myeloid Differentiation Factor 88; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; C485548:UNC13B protein, human