Lower respiratory infections in early life are linked to later asthma

Moraes, Theo J.; Sears, Malcolm R.

doi:10.1136/thoraxjnl-2017-211104

Cited by 8 publications

(7 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the latter study, allergic sensitization did not factor into the associations seen. These data are consistent with the notion that early‐life RV infections induce a nonallergic asthma phenotype . It has also been suggested that early‐life RV infections could drive the development of atopic sensitization and subsequent allergic airways disease …”

Section: Discussionsupporting

confidence: 89%

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

Han

Ishikawa

Bermick

et al. 2020

Allergy

View full text Add to dashboard Cite

Background: Early-life wheezing-associated respiratory infection with human rhinovirus (RV) is associated with asthma development. RV infection of 6-day-old immature mice causes mucous metaplasia and airway hyperresponsiveness which is associated with the expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s) and dependent on IL-25 and IL-33. We examined regulation of this asthma-like phenotype by IL-1β.

show abstract

Section: Discussionsupporting

confidence: 89%

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

Han

Ishikawa

Bermick

et al. 2020

Allergy

View full text Add to dashboard Cite

show abstract

“…Early-life wheezing-associated respiratory tract infections by human rhinovirus (RV) and respiratory syncytial virus (RSV) are considered risk factors for asthma development. [1][2][3][4][5][6][7] Children are infected with many different RV strains, with infants having 6 to 10 distinct RV infections per year. 8 RV infections do not induce specific immunity to reinfection by heterologous serotypes, even if viruses are from the same species (eg, RV-A1A and RV-A2).…”

mentioning

confidence: 99%

“…Recurrent RV infections could result in greater degrees of airway inflammation and the potential for airway remodeling and loss of lung function over time. 5,11,12 In the Tucson Children's Respiratory Study, which is a prospective birth cohort study, lower respiratory tract illness with RSV before 3 years of age was an independent risk factor for the development of wheezing up to age 11 years but not at 13 years. 6 Infants with severe RSV 7 and RV 1 infections requiring hospitalization are more likely to have asthma at ages 13 and 7 years, respectively.…”

mentioning

confidence: 99%

Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype

Rajput

Han

Ishikawa

et al. 2020

Journal of Allergy and Clinical Immunology

View full text Add to dashboard Cite

Early life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype Abbrevations: ILC2s: group 2 innate lymphoid cells RV: human rhinovirus immature mice RV-A1B RV-A2 ILC2 expansion and mucous metaplasia sham RV-A2 day of life 6 13 20 sham RV-A1B no ILC2 expansion or mucous metaplasia ILC2 exaggerated ILC2 expansion and mucous metaplasia ILC2 Background: Early-life wheezing-associated respiratory tract infection by rhinovirus (RV) is a risk factor for asthma development. Infants are infected with many different RV strains per year.Objective: We previously showed that RV infection of 6-day-old BALB/c mice induces a mucous metaplasia phenotype that is dependent on type 2 innate lymphoid cells (ILC2s). We hypothesized that early-life RV infection alters the response to subsequent heterologous infection, inducing an exaggerated asthma-like phenotype. Methods: Wild-type BALB/c mice and Rora fl/fl Il7r cre mice lacking ILC2s were treated as follows: (1) sham on day 6 of life plus sham on day 13 of life, (2) RV-A1B on day 6 plus sham on day 13, (3) sham on day 6 plus RV-A2 on day 13, and (4) RV-A1B on day 6 plus RV-A2 on day 13. Results: Mice infected with RV-A1B at day 6 and sham at day 13 showed an increased number of bronchoalveolar lavage eosinophils and increased expression of IL-13 mRNA but not expression of IFN-g mRNA (which is indicative of a type 2 immune response), whereas mice infected with sham on day 6 and RV-A2 on day 13 of life demonstrated increased IFN-g expression (which is a mature antiviral response). In contrast, mice infected with RV-A1B on day 6 before RV-A2 infection on day 13 showed increased expression of IL-13, IL-5, Gob5,

show abstract

“…A decreased microbial diversity in the gut in 1-week and 1-month-old infants is associated with asthma at 7 years [118]. Gastrointestinal bacterial infections and more general gut dysbiosis early in life may be associated with later asthma and atopy [119,120,121]. Also, patients who later developed asthma showed a skewed composition, with more Clostridia, coliform bacteria, and enterococci as well as less Bacteroidetes, bifidobacteria, and lactobacilli as part of their normal gut microbiota [122].…”

Section: Absence Of Microbesmentioning

confidence: 99%

Special Considerations in Preschool Age

Kere

2019

Severe Asthma in Children and Adolescents

View full text Add to dashboard Cite

Lower respiratory infections in early life are linked to later asthma

Cited by 8 publications

References 15 publications

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype

Special Considerations in Preschool Age

Contact Info

Product

Resources

About