Neonatal hyperoxia promotes asthma-like features through IL-33-dependent ILC2 responses.

ABSTRACT: BACKGROUND:Premature infants often require oxygen supplementation and, therefore, are exposed to oxidative stress. Following oxygen exposure, preterm infants frequently develop chronic lung disease and have a significantly increased risk of asthma. OBJECTIVE:We sought to identify the underlying mechanisms by which neonatal hyperoxia promotes asthma development. METHODS:Mice were exposed to neonatal hyperoxia followed by a period of room air recovery. A group of mice was also intranasally exposed to house dust mite antigen. Assessments were performed at various time points for evaluation of airway hyperresponsiveness, eosinophilia, mucus production, inflammatory gene expression, and TH and group 2 innate lymphoid cell (ILC2) responses. Sera from term- and preterm-born infants were also coll

SUBMITTER: Cheon IS 

PROVIDER: S-EPMC6003836 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature