Abstract

Background and aimBronchiolitis is a leading cause of hospitalization in infants and is associated with a risk of subsequent asthma. The innate immunity genes, such as those encoding toll‐like receptors (TLRs), are likely to play a role in bronchiolitis and post‐bronchiolitis outcome. Thus far, only one study has considered TLR5 genes in respiratory syncytial virus (RSV) bronchiolitis. The aim of this study was to investigate the association of TLR5 gene polymorphism with virus etiology and severity of bronchiolitis, and with post‐bronchiolitis asthma.MethodsWe recruited 164 infants (age < 6 months) hospitalized for bronchiolitis in this study and determined TLR5 rs5744174 (C > T) single nucleotide polymorphism, virus etiology and severity markers of bronchiolitis, and presence of post‐bronchiolitis asthma until age 11 to 13 years.ResultsRSV was detected in 113 (68.9%), rhinovirus in 19 (11.6%), and some other virus in 20 (12.2%) cases. Non‐RSV etiology was more common among infants with the variant CT or TT genotype in the TLR5 rs5744174 gene than in those with the CC genotype (89.7% vs 71.7%, P = 0.03). TLR5 rs5744174 polymorphism was not associated with the need of supplementary oxygen or feeding support, with the length of hospital stay, or with post‐bronchiolitis asthma at any age.ConclusionThe TLR5 rs5744174 variant genotype may increase the susceptibility to bronchiolitis not caused by RSV.

Highlights

  • Asthma is a chronic inflammatory disease of the airways, usually presenting with the dominance of Th2‐type cytokines.[1]

  • We have previously investigated the associations of single‐nucleotide polymorphisms (SNPs) of 9 toll‐like receptors (TLRs) genes, not including the TLR5 gene, with bronchiolitis and post‐bronchiolitis outcome.[23,24,25,26,27]

  • There were no significant associations between the TLR5 rs5744174 genotypes and prolonged cough, inhaled corticosteroids (ICS) use, current asthma, persistent asthma continuing from preschool age until the latest follow‐up visit, or presence of atopic eczema or allergic rhinitis (Table 5.)

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Summary

Introduction

Asthma is a chronic inflammatory disease of the airways, usually presenting with the dominance of Th2‐type cytokines.[1] Both genetic susceptibility and environmental factors, such as early‐life virus infections, contribute to the development of asthma. Still, it remains unclear which abnormalities in the innate immunity ‐based host defense, such as cytokine misproduction, are hereditary, and which develop later due to environmental stress factors, such as infections.[2]. The aim of this study was to investigate the association of TLR5 gene polymorphism with virus etiology and severity of bronchiolitis, and with post‐bronchiolitis asthma. Conclusion: The TLR5 rs5744174 variant genotype may increase the susceptibility to bronchiolitis not caused by RSV

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