title: Evidence for a genetic component in sudden infant death syndrome.
abstract: There is increasing evidence that inflammatory responses have been elicited in some Sudden Infant Death Syndrome (SIDS) infants and that these responses are under genetic control. The objective of this study was to investigate the hypothesis that the cytokine responses of SIDS parents (n = 41) differed significantly from control donors (n = 61). Blood samples were stimulated with the staphylococcal toxin TSST-1 and LPS from Eschericia coli and assessed for production of TNF, IL-1, IL-6, IFN and IL-10. In response toTSST-1 (P < 0.02) and LPS (P < 0.002), SIDS parents produced higher levels of IL-1 than the controls. SIDS parents produced higher levels of IFN in response to TSST-1 compared to LPS (P < 0.001) although in response to LPS, the IFN (P = 0.0008) and IL-6 (P < 0.0002) responses of the SIDS parents were lower than those of the controls. For TNF and IL-10, there was little difference between the two groups unless the effect of smoking was considered. As part of this work, a small pilot genotyping study was carried out using DNA from SIDS parents (n = 10), control donors (n = 10) and Bangladeshi subjects (n = 10). An IFN polymorphism (3/3) was found in 40%,15.4% and 0% of donors respectively. Staphylococcal toxins have been identified in SIDS infants therefore this study highlights the importance of assessing IL-1 levels. Determination of cytokine polymorphisms and consideration of interactions between these and environmental factors such as smoking in high, average and low risk ethnic groups will assist in establishing the contribution of these factors to an infant's susceptibility to SIDS.
authors.affiliation: Medical Microbiology and Forensic Medicine, University of Edinburgh, Edinburgh, UK. a.e.gordon@dundee.ac.uk
authors.forename: A E
authors.initials: AE
authors.lastname: Gordon
authors.forename: D A C
authors.initials: DA
authors.lastname: MacKenzie
authors.forename: O R
authors.initials: OR
authors.lastname: El Ahmer
authors.forename: O M
authors.initials: OM
authors.lastname: Al Madani
authors.forename: J M
authors.initials: JM
authors.lastname: Braun
authors.forename: D M
authors.initials: DM
authors.lastname: Weir
authors.forename: A
authors.initials: A
authors.lastname: Busuttil
authors.forename: C C
authors.initials: CC
authors.lastname: Blackwell
mesh_terms: D001459:Bangladesh; D016022:Case-Control Studies; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007223:Infant; D007249:Inflammation / Q000097:blood / Q000150:complications; D007372:Interferons / Q000097:blood / Q000235:genetics; D007375:Interleukin-1 / Q000097:blood / Q000235:genetics; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D008297:Male; D011110:Polymorphism, Genetic; D013398:Sudden Infant Death / Q000235:genetics*
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D007372:Interferons