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

Figure 8

BRP-39 deletion promotes proinflammatory cytokines in neonatal mice exposed to LPS combined with hyperoxia.  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. Interleukin-6  (IL-6) and IL-1β levels were measured in lung tissue homogenates of indicated treatment groups of WT and BRP-39^−/− mice ((a) and (b)). Each bar represents the mean ± SEM of a minimum of five animals. Results represent three independent experiments. C: control (RA); HYP: hyperoxia; BRP39 KO: BRP39 knock out or BRP-39^−/−. ^∗𝑃<0.05, ^∗∗𝑃<0.01, and ^∗∗∗𝑃<0.001.

(a)

(b)