Hyperoxia Exacerbates Postnatal Inflammation-Induced Lung Injury in Neonatal BRP-39 Null Mutant Mice Promoting the M1 Macrophage Phenotype

Figure 6

BRP-39 deletion enhances mortality in neonatal mice exposed to LPS combined with hyperoxia.  Newborn (NB) BRP-39^−/− or wild-type (WT) mice were exposed to 100% O₂ from postnatal (PN) PN1-7 and survival was assessed. The groups were as follows: WT mice pups treated with lipopolysaccharide (LPS; 𝑛=7), WT mice pups treated with LPS plus hyperoxia (HYP) (𝑛=3), BRP-39^−/− mice pups treated with LPS (𝑛=11), and BRP-39^−/− mice pups treated with LPS plus HYP (𝑛=8). LPS treatment consisted of intranasal administration on alternate days (PN2, -4, and -6) with 3 μg/3 μL in presence or absence of 100% oxygen. ^∗𝑃<0.05.