Figure 1

Acute cigarette smoke model. A. To investigate the relationship between p38 MAPK activation and lung inflammation and injury after CS exposure, C57BL/6 and NZW mice were exposed to air (no-smoke group) or CS for 3 days (n = 6). B-E. Inflammatory cell counts in BALF. BALF total cell (B), macrophage (C) and neutrophil counts (D) were significantly increased by CS exposure in C57BL/6 mice, but to a lesser degree or not at all in NZW mice. BALF lymphocyte counts were significantly decreased by CS exposure in both strains (E). F.G. mRNA expression of inflammatory mediators in the lungs. The expression of 18S rRNA was used as an internal control. mRNA expression levels of TNF-α, MIP-2, and MMP-12 were significantly up-regulated by CS exposure in C57BL/6 mice (F), but to a lesser degree or not at all in NZW mice (G). H. Histological lung differences after CS exposure between C57BL/6 and NZW mice. Mouse lungs exposed to CS demonstrated cell death, seen as cytoplasmic vacuolization (circle) and cytoplasmic blebbing (arrow) of the bronchial epithelium. Acute CS exposure induced these changes in C57BL/6 mice but to a lesser degree in NZW mice. I. J. Apoptosis in the lungs following CS exposure assessed by immunohistochemistry. There were significantly fewer apoptotic cells in NZW mice, as represented by ssDNA (I) and cleaved caspase-3 (J)-positive cells, compared with C57BL/6 mice. K. Oxidative stress following CS exposure evaluated by increased 8-OHdG levels of lung DNA using an ELISA. CS exposure caused a marked increase in 8-OHdG levels of mouse lungs in both strains, but to a lesser extent in NZW than in C57BL/6 mice. *p < 0.05 compared with corresponding non-smoke groups. †p < 0.05 compared with C57BL/6 smoke groups. n = 6 for each experimental set.