Prenatal and postnatal polycyclic aromatic hydrocarbon exposure, airway hyperreactivity, and Beta-2 adrenergic receptor function in sensitized mouse offspring.

ABSTRACT: Despite data associating exposure to traffic-related polycyclic aromatic hydrocarbons (PAH) in asthma, mechanistic support has been limited. We hypothesized that both prenatal and early postnatal exposure to PAH would increase airway hyperreactivity (AHR) and that the resulting AHR may be insensitive to treatment with a β 2AR agonist drug, procaterol. Further, we hypothesized that these exposures would be associated with altered β 2AR gene expression and DNA methylation in mouse lungs. Mice were exposed prenatally or postnatally to a nebulized PAH mixture versus negative control aerosol 5 days a week. Double knockout β 2AR mice were exposed postnatally only. Prenatal exposure to PAH was associated with reduced β 2AR gene expression among nonsensitized mice offspring, but not increases in D

SUBMITTER: Chu S 

PROVIDER: S-EPMC3876588 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature