Figure 4
Pro-inflammatory cytokine, chemokine, and chronic obstructive pulmonary disease (COPD)-related factor messenger RNA (mRNA) expression are reduced and NF-κB p65 activity is inhibited in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-deficient mice exposed to cigarette smoke (CS). Wild-type (WT) or TRAIL-deficient (Tnfsf10−/−) mice were exposed to CS or normal air for 8 weeks. (a) Tumor necrosis factor-α (TNF-α), (b) chemokine (C–C motif) ligand (CCL)2, (c) CCL3, (d) CCL7, (e) CCL12, (f) CCL20, (g) matrix metalloproteinase-12 (MMP-12), and (h) serum amyloid A3 (SAA3) mRNA expression was determined in whole-lung homogenates by qPCR. (i) NF-κB p65 activity in whole-lung homogenates. mRNA data are presented as relative abundance compared with normal air-exposed WT controls. Data (n=5–6) presented as means±s.e.m. are representative of two independent experiments. *P<0.05, **P<0.01; ***P<0.001; ****P<0.0001 compared with normal air-exposed WT or Tnfsf10−/− controls. #P<0.05; ##P<0.01; ###P<0.001; ####P<0.0001 compared with CS-exposed WT controls.
