Hyperoxia Exacerbates Postnatal Inflammation-Induced Lung Injury in Neonatal BRP-39 Null Mutant Mice Promoting the M1 Macrophage Phenotype
BRP-39 modulates LPS induced hyperoxia augmentation of neonatal lung injury.Newborn (NB) BRP-39−/− or wild-type (WT) mice were treated with LPS intranasal administration (3 μg/3 μL) on alternate days (postnatal or PN2, -4, -6) in presence or absence of 100% O2 from PN1–7. Representative photomicrographs of lung histology (H&E stain, 10x) of NB BRP-39−/− or WT mice exposed to room air (RA) or hyperoxia (HYP) or LPS as noted above are shown at PN7 (a). The figures are illustrative of a minimum of 3 animals in each group. Alveolar size, as measured by chord length and septal thickness, confirmed features noted on lung histology ((b) and (c)). Each bar represents the mean ± SEM of a minimum of three animals. Bronchoalveolar lavage (BAL) total cell counts (d) and protein levels (e) of NB BRP-39−/− or WT mice exposed to RA or HYP model, or given treatment as noted above, at PN7. Each bar represents the mean ± SEM of a minimum of three animals. C: control (RA); HYP: hyperoxia; BRP39 KO: BRP39 knock out or BRP-39−/−. , , and .