NADPH Oxidase Limits Innate Immune Responses in the Lungs in Mice
Figure 4
CGD mice develop increased lipopolysaccharide-induced lung inflammation and NF-κB activation compared to wildtype (WT) mice.
Wildtype (WT)/HLL and p47phox−/− /HLL (CGD) mice were administered intratracheal (i.t.) LPS (3 µg/g per mouse). Representative lung histology of a WT/HLL (A) and p47phox−/−/HLL (B) mouse 6 days after i.t. LPS (H&E, 100x). Minimal to no lung inflammation was present in WT/HLL mice, whereas mixed neutrophilic and lymphohistiocytic infiltrates involving ∼10% of the lung and interstitial edema was present in p47phox−/−/HLL mouse lungs. Whole lung NF-κB activation (C) was augmented in p47phox−/−/HLL mice administered i.t. LPS compared to similarly treated WT/HLL mice (2-way ANOVA, p<0.0001, with Bonferroni post-test showing significant differences between genotypes at the indicated time points). D) Isolated p47phox−/−/HLL bone marrow-derived macrophages had augmented NF-κB activation in response to LPS compared to similarly treated WT/HLL macrophages (2-way ANOVA, p<0.0001). *, p<0.05; **, p<0.01; ***, p<0.001.