Abstract
Genetic variants may predispose children to recurrent respiratory infections (RRIs) but studies on genotype-environment interaction are rare. We hypothesized that the risk for RRIs is elevated in children with innate immune gene variants, and that prenatal exposure to maternal psychological distress further increases the risk. In a birth cohort, children with RRIs (n = 96) were identified by the age of 24 months and compared with the remaining cohort children (n = 894). The risk for RRIs in children with preselected genetic variants and the interaction between maternal distress during pregnancy and child genotype were assessed with logistic regression. The IL6 minor allele G was associated with elevated risk for RRIs (OR 1.55; 95% CI 1.14–2.12). Overall, there was no interaction between maternal psychological distress and child genotype. Exploratory analyses showed that, the association between the variant type of IL6 and the risk for RRIs was dependent on prenatal exposure to maternal psychological distress in males (OR 1.96; 95% CI 1.04–3.67). Our study didn’t find genotype-environment interaction between prenatal maternal distress and child genotype. Exploratory analyses suggest sex differences in gene-environment interaction related to susceptibility to RRIs.
Highlights
Genetic variants may predispose children to recurrent respiratory infections (RRIs) but studies on genotype-environment interaction are rare
There are no studies on the interaction of genetic variants of innate immunity and maternal prenatal psychological distress related to Respiratory tract infections (RTIs), it has been previously established that they both alone increase the risk for RRIs
Thirty-one percent of children with RRIs had more than five respiratory infections before the age of 1 year whereas in the comparison group 4% of the children had more than five RTIs
Summary
Genetic variants may predispose children to recurrent respiratory infections (RRIs) but studies on genotype-environment interaction are rare. Polymorphisms of TNF, IL6, and IL10 genes have been reported to affect the susceptibility to RTIs8–11 Environmental risk factors, such as parental smoking during and after p regnancy[12,13], lower socioeconomic status of the family[14], shorter duration of breastfeeding[2,13], (greater) number of s iblings[13], male sex[15], outside-home d aycare[13], and, as recently recognized, maternal psychological distress during pregnancy have been identified to increase the susceptibility to RTIs in children[16,17]. There are no studies on the interaction of genetic variants of innate immunity and maternal prenatal psychological distress related to RTI, it has been previously established that they both alone increase the risk for RRIs
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