Figure 5.

Type I IFN signaling is not necessary for NOX2-deleted mice to develop spontaneous lung inflammation and activated AMs. (A) BAL leukocyte count, percentage of polymorphonuclear leukocytes (PMNs), and total PMNs in 3 mL of BAL from WT, Cybb^KO, Ifnar1^KO, and Cybb^KO Ifnar1^KO mice (n = 12 in each group). (B) Hematoxylin-eosin–stained lung tissues showing the presence of eosinophilic macrophages (arrowhead) and extracellular crystals (arrow) in Cybb^KO and Cybb^KOIfnar1^KO mice. Scale bar, 200 μm and the scale is same for all panels. Representative image from more than 4 samples in each group. (C) qRT-PCR analysis of gene expression in BAL cells isolated from WT, Cybb^KO, Ifnar1^KO, and Cybb^KOIfnar1^KO mice (n = 6 in each group). Bar graph data are expressed as the mean ± standard error of the mean. Experiments were repeated at least twice and the Student t test was performed for samples distributed between 2 groups. *P < .05; **P < .01; ***P < .001; ****P < .0001.