Figure 7
Pulmonary inflammation is suppressed and emphysema-like alveolar enlargement inhibited in experimental chronic obstructive pulmonary disease (COPD) by therapeutic neutralization of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Wild-type mice were exposed to cigarette smoke or normal air for twelve weeks and treated with neutralizing anti-TRAIL monoclonal antibody or isotype control, intraperitoneally three times per week, from week 7 to 12. (a) Total leukocytes, (b) macrophages, (c) neutrophils, and (d) lymphocytes were enumerated in May-Grunwald Giemsa-stained bronchoalveolar lavage (BAL). (e) The numbers of parenchymal inflammatory cells (arrowheads) were determined in periodic acid-Schiff-stained lung sections. (f) NF-κB p65 activity in whole-lung homogenates. (g) Alveolar diameter (μm) was determined in hematoxylin and eosin-stained lung sections using the mean linear intercept technique. (h) The numbers of TUNEL+ (terminal deoxynucleotidyl transferase dUTP nick end labeling) cells (arrowheads) enumerated in whole-lung sections. Data (n=5–6) presented as means±s.e.m. are representative of two independent experiments. **P<0.01; ***P<0.001; ****P<0.0001 compared with isotype-treated or anti-TRAIL-treated normal air-exposed controls. #P<0.05; ##P<0.01; ###P<0.001; ####P<0.0001 compared with isotype-treated CS-exposed controls.
