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

Figure 4

BRP-39 deletion promotes the M1 phenotype in macrophages. Enhanced expression of M1 marker genes, inducible nitric oxide synthase (iNOS), and interleukin-6 (IL-6) mRNA expression in BRP-39^−/− peritoneal macrophages stimulated by lipopolysaccharide (LPS; 100 ng/mL) for 16 h ((a) and (b)). Western blot and densitometry showing increased iNOS protein expression in BRP-39^−/− bone marrow derived macrophages (BMDMs) stimulated by LPS (100 ng/mL) or LPS plus hyperoxia for 24 h (c). BRP-39^−/− BMDMs generate increased IL-6 after LPS (100 ng/mL) stimulation for 16 h as compared to wild type (WT) (d). Results expressed as the mean ± SEM; 𝑛=3, in each group. 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)

(c)

(d)