Abstract
Bronchiolitis is the most common cause of hospitalization in infancy and is associated with a higher risk for the development of childhood asthma. However, not all children hospitalized with bronchiolitis will develop asthma. The mechanisms underlying asthma development following bronchiolitis hospitalization are complex. Immune responses to respiratory viruses may underlie both bronchiolitis severity and long-term sequela (such as asthma). Interferons (IFNs) are important components of innate immune responses to respiratory viruses and could influence both asthma development and asthma exacerbations. However, the nature of the relationship between interferon production and wheezing illnesses is controversial. For example, low peripheral blood IFN responses at birth have been linked with recurrent wheeze and asthma development. In contrast, there is evidence that severe illnesses (e.g., hospitalization for bronchiolitis) are associated with increased IFN responses during acute infection (bronchiolitis hospitalization) and a higher risk for subsequent asthma diagnosis. Furthermore, mechanistic studies suggest that bronchial epithelial cells from asthmatic children have impaired IFN responses to respiratory viruses, which may enable increased viral replication followed by exaggerated secondary IFN responses. This review aims to discuss controversies around the role of IFNs as drivers of susceptibility to asthma development following bronchiolitis hospitalization. Past evidence from both mechanistic and cohort studies are discussed. We will highlight knowledge gaps that can inform future research study design.
Highlights
Bronchiolitis remains the most common lower respiratory tract infection in infancy [1, 2]
Other studies showed that respiratory syncytial virus (RSV) and RV bronchiolitis induce specific type III IFN subtypes that correlate with disease severity [31]
Data from upper airway samples show that in infants hospitalized with bronchiolitis, upregulated IFN transcription and increased type III IFN secretion during the acute infection is associated with higher risk for recurrent wheeze and asthma
Summary
Bronchiolitis remains the most common lower respiratory tract infection in infancy [1, 2]. Several reports have associated specific viruses, such as respiratory syncytial virus (RSV) and rhinovirus (RV) with an increased risk of recurrent wheeze and asthma diagnosis [6, 9] These associations may not be causal; they are potentially mediated by other factors (such as genetic predisposition and host immune responses) [10]. Innate IFNs seem to play an important role in bronchiolitis pathogenesis, and in defining risk for subsequent chronic airway disease (recurrent wheeze, asthma) [15, 20] It is important to have a comprehensive understanding of the existing evidence with the aim to highlight controversies and knowledge gaps This narrative scoping review aims to identify gaps in our understanding around the reported role of IFNs as mediators of susceptibility to subsequent asthma following hospitalization for bronchiolitis. Following scoping of the literature, we present the synthesis of the evidence from both cohort and mechanistic studies
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
