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1.
Front Immunol ; 12: 761660, 2021.
Article in English | MEDLINE | ID: mdl-34925333

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.


Subject(s)
Asthma/immunology , Bronchiolitis/immunology , Interferons/immunology , Animals , Cohort Studies , Disease Susceptibility , Humans
3.
Microbes Infect ; 14(6): 495-9, 2012 Jun.
Article in English | MEDLINE | ID: mdl-22285902

ABSTRACT

Airway epithelial cells are the main cells infected by respiratory viruses including rhinoviruses and respiratory syncytial virus. Virus modulation of inhibitory molecule PD-L1 on epithelial cells may be important in limiting anti-viral effector CD8(+) T cell responses and, consequently, worsening acute virus-induced lung tissue damage.


Subject(s)
B7-H1 Antigen/metabolism , Programmed Cell Death 1 Receptor/metabolism , Respiratory Syncytial Virus, Human/immunology , Respiratory Tract Infections/immunology , Rhinovirus/pathogenicity , Animals , CD8-Positive T-Lymphocytes/immunology , Child , Child, Preschool , Epithelial Cells/immunology , Epithelial Cells/virology , Humans , Infant , Lung/cytology , Lung/immunology , Lung/virology , Mice , Mice, Inbred BALB C , Respiratory Syncytial Virus, Human/pathogenicity , Respiratory Tract Infections/virology , Rhinovirus/immunology
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