Il-10 gene polymorphisms are associated with infectious cause of sudden infant death

Abstract

Cytokines are involved in regulating the intensity and duration of the immune response, and cytokine production is carefully regulated. With regard to sudden infant death, interleukin-10 (IL-10) is of special interest. This is an immunregulatory cytokine that plays an important role in the development of infectious disease. The purpose of this study was to elucidate the relationship between polymorphisms in the promoter region of the IL-10 gene and sudden infant death due to either sudden infant death syndrome (SIDS) or infection. The polymorphisms investigated include the SNPs in base pairs (bp) -1082, -819, -592, and the two microsatellites IL-10G and IL-10R. The main finding is an association between the ATA haplotype and the ATA/ATA genotype and infectious death. The group of infectious deaths also had a higher percentage of the genotypes G21/G22 and G21/G23, compared with the SIDS patients. In addition, G21/G22 was found in a higher percentage of the SIDS patients than in the controls. These findings lead us to speculate that, in some situations, an infant with an unfavorable IL-10 genotype may exhibit aberrant IL-10 production, which in turn leads to an imbalance in the immune response and renders the infant unable to cope with the infection.