The first definition of bronchiolitis was given more than 80 years ago. Since then, efforts have been made to describe differences in clinical findings and to associate these differences with acute and chronic outcomes (most commonly asthma). Furthermore, several randomized controlled trials have attempted to provide data on the impact of bronchiolitis treatments on both acute and chronic outcomes (e.g., asthma development). Data from these studies failed to identify a new direction for treatment and prevention, mainly due to holding to the false assumption that bronchiolitis is a single disease entity.
The encouraging news is that a period of change in bronchiolitis prevention and management is coming. Precision epidemiology is providing the ability to combine high-quality respiratory virus diagnostics and environmental and biological data with patient outcomes. In this way, physicians are able to map the trajectory of the disease and apply tailored treatments to individual patients. These approaches pay sufficient attention to the heterogeneity of the pathophysiology of the disease, its clinical presentation, and the response to treatment.
Current literature collectively suggests that bronchiolitis is not a single disease and the distribution of risk for asthma development in the population of infants with bronchiolitis follows a continuum that ranges from infants who do not have risk factors for asthma development and do not develop asthma to infants who have persistent relapses with wheeze symptoms following bronchiolitis and receive an asthma diagnosis at early school years.
Genetic studies of susceptibility to bronchiolitis have identified variants in selected candidate genes, often related to immunity, being associated with increased susceptibility to severe bronchiolitis. A few studies have evaluated the relevance of larger groups of genes and have linked variations in the severity of bronchiolitis with innate immunity–related genes (IL13, IL4 locus in the 5q31 cytokine cluster). Variants in genes encoding proteins, such as toll-like receptors (TLRs), surfactant protein D (SFTPD), and Vitamin D receptor (VDR), have also been associated with increased susceptibility to severe bronchiolitis.
In addition to these findings, polymorphisms in genes (IL-10, IL-13, TLR4, VDR, CCR5, and ADAM33) have been associated with both increased incidence of bronchiolitis and subsequent asthma. For example, an increased risk of childhood-onset asthma after rhinovirus infection has been associated with the 17q21 locus.
In regard to the role of the epigenome in defining susceptibility to severe bronchiolitis and asthma, there are few studies associating changes in peripheral blood and nasal airway RNA- and non-RNA-based post-transcriptional regulation with asthma development. However, there is no data from epigenome-wide association studies (EWAS) in regard to bronchiolitis.
Although these studies have provided significant evidence, there are still important research gaps. By utilizing data science approaches in the integration of multiple “omics” data, we aim to bridge these gaps and improve our understanding of asthma development following the most common lower respiratory infection in infancy, bronchiolitis.
This Research Topic aims to bring together basic scientists and clinicians whose research is focusing on immunology, virology, genetics, epigenetics, and precision epidemiology research to shed more light on the bronchiolitis to asthma development pathway. The research studies that are invited to this Research Topic will not focus only on “multi-omics” research, but will provide compelling evidence that will drive future “multi-omics” approaches.
More specifically, we welcome the submission of studies that fall within the following categories:
1. Observational studies investigating the inter-relationship between respiratory viruses, genome, epigenome and/or transcriptome and subsequent asthma development
2. Genetics research studies that focus on identifying genetic determinants of asthma in infants with severe bronchiolitis
3. Epigenetics research studies that focus on identifying associations between epigenetic marks and asthma in infants with severe bronchiolitis
4. Randomized controlled trials with a cohort design that explore new therapeutic targets in severe bronchiolitis and their impact on asthma prevention
5. Experimental studies investigating mechanisms that underlie susceptibility to asthma development following bronchiolitis (in vivo and ex vivo mechanistic studies)
6. Systematic reviews and/or meta-analyses on topics 1 to 5
The first definition of bronchiolitis was given more than 80 years ago. Since then, efforts have been made to describe differences in clinical findings and to associate these differences with acute and chronic outcomes (most commonly asthma). Furthermore, several randomized controlled trials have attempted to provide data on the impact of bronchiolitis treatments on both acute and chronic outcomes (e.g., asthma development). Data from these studies failed to identify a new direction for treatment and prevention, mainly due to holding to the false assumption that bronchiolitis is a single disease entity.
The encouraging news is that a period of change in bronchiolitis prevention and management is coming. Precision epidemiology is providing the ability to combine high-quality respiratory virus diagnostics and environmental and biological data with patient outcomes. In this way, physicians are able to map the trajectory of the disease and apply tailored treatments to individual patients. These approaches pay sufficient attention to the heterogeneity of the pathophysiology of the disease, its clinical presentation, and the response to treatment.
Current literature collectively suggests that bronchiolitis is not a single disease and the distribution of risk for asthma development in the population of infants with bronchiolitis follows a continuum that ranges from infants who do not have risk factors for asthma development and do not develop asthma to infants who have persistent relapses with wheeze symptoms following bronchiolitis and receive an asthma diagnosis at early school years.
Genetic studies of susceptibility to bronchiolitis have identified variants in selected candidate genes, often related to immunity, being associated with increased susceptibility to severe bronchiolitis. A few studies have evaluated the relevance of larger groups of genes and have linked variations in the severity of bronchiolitis with innate immunity–related genes (IL13, IL4 locus in the 5q31 cytokine cluster). Variants in genes encoding proteins, such as toll-like receptors (TLRs), surfactant protein D (SFTPD), and Vitamin D receptor (VDR), have also been associated with increased susceptibility to severe bronchiolitis.
In addition to these findings, polymorphisms in genes (IL-10, IL-13, TLR4, VDR, CCR5, and ADAM33) have been associated with both increased incidence of bronchiolitis and subsequent asthma. For example, an increased risk of childhood-onset asthma after rhinovirus infection has been associated with the 17q21 locus.
In regard to the role of the epigenome in defining susceptibility to severe bronchiolitis and asthma, there are few studies associating changes in peripheral blood and nasal airway RNA- and non-RNA-based post-transcriptional regulation with asthma development. However, there is no data from epigenome-wide association studies (EWAS) in regard to bronchiolitis.
Although these studies have provided significant evidence, there are still important research gaps. By utilizing data science approaches in the integration of multiple “omics” data, we aim to bridge these gaps and improve our understanding of asthma development following the most common lower respiratory infection in infancy, bronchiolitis.
This Research Topic aims to bring together basic scientists and clinicians whose research is focusing on immunology, virology, genetics, epigenetics, and precision epidemiology research to shed more light on the bronchiolitis to asthma development pathway. The research studies that are invited to this Research Topic will not focus only on “multi-omics” research, but will provide compelling evidence that will drive future “multi-omics” approaches.
More specifically, we welcome the submission of studies that fall within the following categories:
1. Observational studies investigating the inter-relationship between respiratory viruses, genome, epigenome and/or transcriptome and subsequent asthma development
2. Genetics research studies that focus on identifying genetic determinants of asthma in infants with severe bronchiolitis
3. Epigenetics research studies that focus on identifying associations between epigenetic marks and asthma in infants with severe bronchiolitis
4. Randomized controlled trials with a cohort design that explore new therapeutic targets in severe bronchiolitis and their impact on asthma prevention
5. Experimental studies investigating mechanisms that underlie susceptibility to asthma development following bronchiolitis (in vivo and ex vivo mechanistic studies)
6. Systematic reviews and/or meta-analyses on topics 1 to 5
