IL-1 gene cluster polymorphisms and sudden infant death syndrome

Ferrante, Linda; Opdal, Siri Hauge; Vege, Åshild; Rognum, Torleiv O.

doi:10.1016/j.humimm.2010.01.011

Cited by 19 publications

(12 citation statements)

References 33 publications

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“…However, this could not be confirmed in a Norwegian study of 175 SIDS cases [29]. Since then, Ferrante et al have investigated in total 10 different SNPs in the genes encoding IL-1, IL-6, IL-8, IL-12, IL-13 IL-16, and IL-18, as well as one VNTRs in each of the genes encoding IL-1a and IL-1Ra [33,34] in 204 Norwegian SIDS cases and in 131 adult diseased controls. The only association that was found with SIDS was for the gene combination IL-1a VNTR A1A1/IL-1b ?4845TT (P \ 0.01), a gene combination one could expect to result in a decreased level of IL-1a [33].…”

Section: Immune Systemmentioning

confidence: 95%

“…The cytokines regulate the intensity and duration of the immune response by stimulating the different cells involved, and thus activates a network of interacting cells . The interleukin genes investigated with regard to SIDS so far are those encoding for IL-1a, IL-1b, IL-4, IL-6, IL-10, IL-12, IL-13, IL-16, IL-18, transforming growth factor (TGF), tumor necrosis factor a (TNFa), and interferon gamma (IFNc) [22][23][24][25][26][27][28][29][30][31][32][33][34].…”

Section: Immune Systemmentioning

confidence: 99%

“…Since then, Ferrante et al have investigated in total 10 different SNPs in the genes encoding IL-1, IL-6, IL-8, IL-12, IL-13 IL-16, and IL-18, as well as one VNTRs in each of the genes encoding IL-1a and IL-1Ra [33,34] in 204 Norwegian SIDS cases and in 131 adult diseased controls. The only association that was found with SIDS was for the gene combination IL-1a VNTR A1A1/IL-1b ?4845TT (P \ 0.01), a gene combination one could expect to result in a decreased level of IL-1a [33]. Associations were also found between genotype and sleeping position, as the genotypes IL-18 -251AA/AT, IL-8 -781 CT/TT, and IL-1b -511CC/CT were more frequent in SIDS cases found prone.…”

Section: Immune Systemmentioning

confidence: 99%

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Gene variants predisposing to SIDS: current knowledge

Opdal

Rognum

2010

Forensic Sci Med Pathol

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Genetic risk factors play a role in sudden unexpected infant death; either as a cause of death, such as in cases with medium-chain acyl-coenzyme A dehydrogenase deficiency and cardiac arrest due to long QT syndrome, or as predisposing factors for sudden infant death syndrome (SIDS). Most likely genetic predisposition to SIDS represent a polygenic inheritance pattern leading to sudden death when combined with other risk factors, such as a vulnerable developmental stage of the central nervous system and/or the immune system, in addition to environmental risk factors, such as a common cold or prone sleeping position. Genes involved in the regulation of the immune system, cardiac function, the serotonergic network and brain function and development have so far emerged as the most important with respect to SIDS. The purpose of the present paper is to survey current knowledge on SIDS and possible genetic contributions.

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Section: Immune Systemmentioning

confidence: 95%

Section: Immune Systemmentioning

confidence: 99%

Section: Immune Systemmentioning

confidence: 99%

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Gene variants predisposing to SIDS: current knowledge

Opdal

Rognum

2010

Forensic Sci Med Pathol

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“…Molecular studies have disclosed several polymorphisms located in immune genes that are associated with SIDS, including genes encoding complement component C4 and several interleukins (30)(31)(32)(33)(34)(35). Considering this immunological vulnerability in SIDS, it is possible that some infants do not have the biological capacity to fight an infection in an effective manner.…”

Section: Mrna Expression In Sidsmentioning

confidence: 99%

Altered gene expression and possible immunodeficiency in cases of sudden infant death syndrome

et al. 2016

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Background: 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. Methods: 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. results: 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. conclusion: 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.

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“…A study of the same IL-1RN VNTR polymorphism was recently published by Ferrante et al 26 reporting no association between any IL-1RN VNTR genotype and SIDS infants who died in Norway. The infants studied were from the same period (1987/88 to 2006) and exhibited almost the same percentages of A2 homozygous SIDS and control infants as the present study, 15% SIDS with 2/2 in Ferrante's study versus 15.9% in the present study, and 7% controls with 2/2 in Ferrante's study versus 9.6% in the present study.…”

Section: Discussionmentioning

confidence: 83%