Document Detail


Evidence for a genetic component in sudden infant death syndrome.
MedLine Citation:
PMID:  12515435     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
A E Gordon; D A C MacKenzie; O R El Ahmer; O M Al Madani; J M Braun; D M Weir; A Busuttil; C C Blackwell
Related Documents :
7523575 - Sudden infant death syndrome: a possible primary cause.
25044665 - Tobacco control policies and sudden infant death syndrome in developed nations.
17314115 - Size for gestational age at birth: impact on risk for sudden infant death and other cau...
19090325 - Qt interval prolongation in future sids victims: a polysomnographic study.
10591435 - Persistent value of air-augmented radiograph in neonatal high gastrointestinal obstruct...
19396605 - Association of escherichia coli o157:h7 with necrotizing enterocolitis in a full-term i...
Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Child: care, health and development     Volume:  28 Suppl 1     ISSN:  0305-1862     ISO Abbreviation:  Child Care Health Dev     Publication Date:  2002 Sep 
Date Detail:
Created Date:  2003-01-07     Completed Date:  2003-01-31     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7602632     Medline TA:  Child Care Health Dev     Country:  England    
Other Details:
Languages:  eng     Pagination:  27-9     Citation Subset:  IM    
Affiliation:
Medical Microbiology and Forensic Medicine, University of Edinburgh, Edinburgh, UK. a.e.gordon@dundee.ac.uk
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Bangladesh
Case-Control Studies
Cytokines / biosynthesis
Female
Genetic Predisposition to Disease
Genotype
Humans
Infant
Inflammation / blood,  complications
Interferons / blood,  genetics
Interleukin-1 / blood,  genetics
Interleukin-6 / blood,  genetics
Male
Polymorphism, Genetic
Sudden Infant Death / genetics*
Chemical
Reg. No./Substance:
0/Cytokines; 0/Interleukin-1; 0/Interleukin-6; 9008-11-1/Interferons

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Why is smoking a risk factor for sudden infant death syndrome?
Next Document:  Hair-element analysis--still on the fringe.