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

Figure 7

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^−/−. ^∗𝑃<0.05, ^∗∗𝑃<0.01, and ^∗∗∗𝑃<0.001.

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