Toll-like receptor 1 and 10 variations increase asthma risk and review highlights further research directions.
Bronchiolitis
Childhood asthma
Innate immunity
Polymorphism
Toll-like receptor
Journal
Acta paediatrica (Oslo, Norway : 1992)
ISSN: 1651-2227
Titre abrégé: Acta Paediatr
Pays: Norway
ID NLM: 9205968
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
19
02
2019
revised:
19
03
2019
accepted:
25
03
2019
pubmed:
30
3
2019
medline:
2
9
2020
entrez:
30
3
2019
Statut:
ppublish
Résumé
This paper summarises variations in the genes encoding toll-like receptors (TLRs) in relation to the aetiology and outcome of infant bronchiolitis. It compares the literature with research carried out by our group. A mini review was conducted to provide context for a study carried out at the Department of Paediatrics, Tampere University Hospital, Finland. In 2000-2004, 187 infants were hospitalised for bronchiolitis and then followed up: 129 at 1.5 years of age, 166 at 5-7 years of age and 138 at 11-13 years of age. The review showed that the Finnish bronchiolitis study was the only prospective study on the association between TLRs and the emergence of childhood asthma or lung function reduction after bronchiolitis in infancy. It found that TLR1 and TLR10 variant genotypes were associated with more asthma at 5-7 and 11-13 years, with inconsistent results for the other eight TLR genes. Large population-based studies were also identified that stressed the importance of the TLR2 subfamily members in childhood asthma. Our study found that variations in the TLR1 and TLR10 genes increased the asthma risk after bronchiolitis. The mini review calls for further research on the TLR2 subfamily in bronchiolitis and childhood asthma.
Substances chimiques
TLR1 protein, human
0
TLR10 protein, human
0
Toll-Like Receptor 1
0
Toll-Like Receptor 10
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1406-1410Informations de copyright
©2019 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.