Document Detail

Interleukin-10 and sudden infant death syndrome.
MedLine Citation:
PMID:  15325406     Owner:  NLM     Status:  MEDLINE    
Uncontrolled pro-inflammatory responses to infections or bacterial toxins have been suggested to play a role in triggering the physiological events leading to sudden infant death syndrome (SIDS). We tested the hypothesis that these uncontrolled responses might be due to interactions between the gene polymorphisms inducing low levels of IL-10 and exposure to cigarette smoke. In vitro, the IL-10 (G-1082A) polymorphism was associated with low IL-10 levels and the -1082G allele was associated with high levels. The first objective was to assess the distribution of this polymorphism among SIDS infants, parents of SIDS infants and controls, and two ethnic groups: Aboriginal Australians who have a high incidence of SIDS; and Bangladeshis who in Britain have a low incidence of SIDS compared with Europeans. The second objective was to assess effects of human recombinant IL-10 on interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) responses of human leukocytes to staphylococcal toxins implicated in SIDS. The third objective was to assess IL-10 responses to endotoxin and toxic shock syndrome toxin (TSST) from leukocytes of smokers and non-smokers in relation to the IL-10 (G-1082A) polymorphism. There were major differences in the distributions of these polymorphisms between Europeans and Bangladeshis (p=0.00) and between Europeans and Aboriginal Australians (p=0.00); however, they were similar for the Bangladeshi and Aboriginal Australian subjects. There were no significant differences in the distribution of these polymorphisms among SIDS infants or parents of SIDS infants compared to control groups. IL-10 significantly reduced IL-6 and TNF-alpha responses to TSST and staphylococcal enterotoxins A and C. At 50 ng ml(-1), IL-10 significantly increased TNF-alpha but not IL-6 responses to TSST and enterotoxin A. Although IL-10 responses to endotoxin were lower from leukocytes of smokers who were homozygous for the G allele, the differences were not significant; however, significantly lower IL-10 responses were found for smokers who were homozygous for the A allele (p=0.01) and heterozygotes (p=0.04). The pooled data found smokers had significantly lower levels of IL-10 responses to TSST, but there were no significant differences for smokers compared with non-smokers for the three genotypes. The high incidence of SIDS and serious respiratory infections among Aboriginal Australian infants and the low incidence of these conditions among Bangladeshi infants might be explained in part by our findings of differences in IL-10 responses between smokers and non-smokers. The lowest levels of IL-10 responses were observed among smokers who were homozygous for the A allele which is most prevalent among the Aboriginal Australians (83%) and Bangladeshis (84%). The major difference between the risk factors for SIDS in these two groups is the level of exposure of infants to cigarette smoke associated with maternal smoking.
Sophia M Moscovis; Ann E Gordon; Osama M Al Madani; Maree Gleeson; Rodney J Scott; June Roberts-Thomson; Sharron T Hall; Donald M Weir; Anthony Busuttil; C Caroline Blackwell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  FEMS immunology and medical microbiology     Volume:  42     ISSN:  0928-8244     ISO Abbreviation:  FEMS Immunol. Med. Microbiol.     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-08-24     Completed Date:  2004-10-28     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9315554     Medline TA:  FEMS Immunol Med Microbiol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  130-8     Citation Subset:  IM    
School of Biomedical Sciences, Faculty of Health, University of Newcastle, and Hunter Medical Research Institute, Newcastle, NSW, Australia.
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MeSH Terms
Continental Population Groups
Gene Frequency
Genetic Predisposition to Disease*
Interleukin-10 / genetics*
Polymorphism, Single Nucleotide*
Risk Factors
Sudden Infant Death / epidemiology,  genetics*
Reg. No./Substance:

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