Genetic ablation of Nrf2 enhances susceptibility to cigarette smoke–induced emphysema in mice
J. Clin. Invest. Tirumalai Rangasamy, et al. 114:1248 doi:10.1172/JCI21146 [
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Figure 5Increased inflammation in the lungs of CS-exposed
Nrf2–/– mice. (
A) Lavaged inflammatory cells from control and CS-exposed mice. The number of macrophages in BAL fluid collected from the CS-exposed (both 1.5 months and 6 months)
Nrf2–/– mice was significantly higher than in the BAL fluid from CS-exposed
Nrf2+/+ mice and the respective age-matched control mice. Values represent mean ± SEM (
n = 8). PMNs, polymorphonuclear leukocytes. *
P – 0.05 vs. control of the same genotype;
P – 0.05 across the genotypes in CS-exposed group. (
B) Immunohistochemical detection of macrophages (arrows) in lungs of
Nrf2+/+ and
Nrf2–/– mice exposed to CS for 6 months. Magnification, ×40. Scale bars: 25 μm. (
C) Quantification of macrophages in lungs after 6 months of CS exposure. The lung sections from the CS-exposed
Nrf2–/– mice showed significantly more macrophages than did those from wild-type counterparts exposed to CS (**
P – 0.025). However, there was no significant difference in the number of alveolar macrophages between the air-exposed
Nrf2+/+ and
Nrf2–/– mice (
P > 0.9).
