
doi: 10.1111/ped.14746
pmid: 33877723
AbstractBackgroundToll‐interacting protein is a key factor in regulating innate immunity responses via gatekeeping Toll‐like receptors. Genetic variance in innate immunity has been linked with susceptibility to infections. Children with viral bronchiolitis in infancy are at increased risk of later asthma. The aim was to evaluate the role of toll‐interacting protein gene point mutations in severity of bronchiolitis and subsequent risk of asthma.MethodsInfants less than 6 months old were recruited during hospitalization due to bronchiolitis. In all, 166 children were prospectively followed up to age of 1.5, 6, and 11 years. Clinical data on viral etiology and severity markers, and further post‐bronchiolitis asthma and lung function outcomes were compared with genetic differences in two single‐nucleotide point mutations rs116938768 and rs5743854 in the toll‐interacting protein gene.ResultsToll‐interacting protein rs116938768 or rs5743854 did not show significant associations with severity markers or viral etiology of bronchiolitis. Follow‐up data on current asthma or lung function at 6 or 11 years of age after bronchiolitis were not associated with the investigated mutations.ConclusionToll‐interacting protein gene point mutations in rs116938768 or rs5743854 were not involved with the clinical course of viral bronchiolitis in early infancy, and did not predict post‐bronchiolitis asthma or lung function reduction by the age of 11 years.
3123, Polymorphism, Genetic, Intracellular Signaling Peptides and Proteins, 610, Infant, 3121 Internal medicine, ta3111, Asthma, 3121, Hospitalization, 3123 Gynaecology and paediatrics, Child, Preschool, Bronchiolitis, Viral, Humans, Child
3123, Polymorphism, Genetic, Intracellular Signaling Peptides and Proteins, 610, Infant, 3121 Internal medicine, ta3111, Asthma, 3121, Hospitalization, 3123 Gynaecology and paediatrics, Child, Preschool, Bronchiolitis, Viral, Humans, Child
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