Sudden Infant Death Syndrome Research Today is a free monthly online journal that collates and summarizes the latest research about Sudden Infant Death Syndrome, including details on sids, causes, prevention, statistics. | ||||||||
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IL6 G-174C Associated With Sudden Infant Death Syndrome in a Caucasian Australian Cohort.Moscovis SM, Gordon AE, Al Madani OM, Gleeson M, Scott RJ, Roberts-Thomson J, Hall ST, Weir DM, Busuttil A, Blackwell CC School of Biomedical Sciences, Faculty of Health, University of Newcastle, and Hunter Medical Research Institute, Newcastle, NSW, Australia. The aims of this study were to analyze IL6 G-174C in relation to high interleukin (IL)-6 concentrations found in some sudden infant death syndrome (SIDS) infants, and to assess the effects of IL6 G-174C, smoking status, and gender on IL-6 responses. SIDS infants, parents of SIDS infants, and populations with high (Aboriginal Australian), medium (Caucasian) or low (Bangladeshi) SIDS incidences were genotyped. Leukocytes were stimulated in vitro with endotoxin and IL-6 responses were assessed in relation to IL6 G-174C genotype, smoking status, and gender. The study findings showed that GG genotype, associated with high IL-6 responses, was predominant among Australian SIDS infants (58%) compared with control subjects (38%, p = 0.02), as well as Bangladeshis (94%) and Aboriginal Australians (88%) compared with Caucasians (42%, p < 0.01). GC smokers had higher median IL-6 responses (8.4 ng/ml(-1)) than GG (3.5 ng/ml(-1), p = 0.01) or CC smokers (2.4 ng/ml(-1), p < 0.01). GG nonsmokers had higher median IL-6 responses (4.9 ng/ml(-1)) than GG smokers (p < 0.05). Gender did not affect IL-6 responses. In conclusion, an association between IL6 G-174C and Australian SIDS infants was observed. IL6 G-174C alone cannot explain observed differences in the incidence of SIDS in the Bangladeshi and Aboriginal Australian populations. Further investigations are needed on interactions between smoking and gene polymorphisms in relation to proinflammatory responses implicated in SIDS. Published 23 October 2006 in Hum Immunol, 67(10): 819-25.
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