Document Detail

Interleukin 1-beta responses to bacterial toxins and sudden infant death syndrome.
MedLine Citation:
PMID:  15325407     Owner:  NLM     Status:  MEDLINE    
We tested the hypothesis that significantly higher IL-1beta responses to toxic shock syndrome toxin (TSST) noted for parents of sudden infant death syndrome (SIDS) infants might be due in part to genetic factors such as the IL-1beta (C-511T) and IL-1RN (T+2018C) single nucleotide polymorphisms (SNP). The first objective was to assess the distribution of these polymorphisms 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 IL-1beta responses to endotoxin and toxic shock syndrome toxin (TSST) from leukocytes of smokers and non-smokers in relation to these polymorphisms. There were major differences in the distributions of the IL-1beta (C-511T) SNP 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. The allele frequency distribution of the IL-1RN (T+2018C) SNP for the Aboriginal Australians was statistically different from the European group (p=0.00), but it was not different from the Bangladeshi group (p=0.09). Compared with controls of European origin, there were no significant differences in the distribution of these polymorphisms among SIDS infants or parents of SIDS infants. For the IL-1beta (C-511T) SNP, the highest IL-1beta responses to endotoxin were obtained with leukocytes of non-smokers with the heterozygous CT genotype. Smokers had significantly lower levels of IL-1beta in response to endotoxin (p=0.01) and these differences were significant for donors with the wild type CC (p=0.00) and CT (p=0.03) genotypes. Similar patterns were observed for IL-1beta responses to TSST, but the differences were not significant. For the IL-1RN (T+2018C) SNP, the highest IL-1beta responses to endotoxin were obtained with leukocytes from non-smoker donors with the wildtype TT genotype and significantly lower responses were found with leukocytes from donors with the TC genotype (p=0.02). The responses of smokers were lower but the differences were significant only for donors with the TT genotype (p=0.00). Similar patterns were observed for IL-1beta responses to TSST, but the differences were not significant. IL-1beta responses to both endotoxin and TSST were increased for the small number of smokers with the TT genotype of the IL-1beta (C-511T) SNP. The TT genotype of the IL-1beta (C-511T) was found predominantly among Aboriginal Australian and Bangladeshi individuals but only a small proportion of Europeans. Smokers with the AA genotype of the IL-10 (G-1082A) SNP which is found predominantly among these two groups had significantly lower levels of IL-10 responses. If cigarette smoke enhances pro-inflammatory responses and reduces anti-inflammatory responses in individuals with these genotypes, this might partly explain the increased susceptibility of Aboriginal Australian infants to infections and SIDS.
Sophia M Moscovis; Ann E Gordon; Sharron T Hall; Maree Gleeson; Rodney J Scott; June Roberts-Thomsom; 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:  139-45     Citation Subset:  IM    
School of Biomedical Sciences, Faculty of Health, Immunology and Microbiology, David Maddison Building, University of Newcastle, Newcastle, NSW 2300, Australia.
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MeSH Terms
Bacterial Toxins / immunology*
Continental Population Groups
Enterotoxins / immunology
Gene Frequency
Genetic Predisposition to Disease
Interleukin-1 / genetics*,  metabolism*
Leukocytes / immunology
Polymorphism, Single Nucleotide*
Receptors, Interleukin-1 / genetics
Sudden Infant Death / epidemiology,  genetics,  immunology*
Superantigens / immunology
Reg. No./Substance:
0/Bacterial Toxins; 0/Enterotoxins; 0/Interleukin-1; 0/Receptors, Interleukin-1; 0/Superantigens; 0/enterotoxin F, Staphylococcal

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