| Interleukin 1-beta responses to bacterial toxins and sudden infant death syndrome. | |
| | |
MedLine Citation:
|
PMID: 15325407 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
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. |
| | |
Authors:
|
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 |
Related Documents
:
|
9042127 - Comparison of two methods of determining asphyxial potential of infant bedding. 21075317 - Bed sharing among black infants and sudden infant death syndrome: interactions with oth... 8707947 - Significance of endotoxin in lethal synergy between bacteria associated with sudden inf... 11394337 - Sudden unexpected infant deaths in dundee, 1882-1891: overlying or sids? 10541327 - Granulocyte-macrophage colony-stimulating factor increases surfactant phospholipid in p... 15513157 - Cerebral asymmetry of emotion and its relationship to olfaction in infancy. |
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 |
Affiliation:
|
School of Biomedical Sciences, Faculty of Health, Immunology and Microbiology, David Maddison Building, University of Newcastle, Newcastle, NSW 2300, Australia. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Bacterial Toxins
/
immunology* Continental Population Groups Enterotoxins / immunology Gene Frequency Genetic Predisposition to Disease Humans Infant Interleukin-1 / genetics*, metabolism* Leukocytes / immunology Polymorphism, Single Nucleotide* Receptors, Interleukin-1 / genetics Smoking Sudden Infant Death / epidemiology, genetics, immunology* Superantigens / immunology |
| Chemical | |
Reg. No./Substance:
|
0/Bacterial Toxins; 0/Enterotoxins; 0/Interleukin-1; 0/Receptors, Interleukin-1; 0/Superantigens; 0/enterotoxin F, Staphylococcal |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Interleukin-10 and sudden infant death syndrome.
Next Document: Motion velocity thresholds in deaf signers: changes in lateralization but not in overall sensitivity...