Figure 1.
Tobacco smoke induced damage to the lung.
Cigarette smoke-induced damage was evaluated in hematoxylin stained lung tissue sections (top). Cigarette smoke-induced neutrophil infiltration was evaluated using myeloperoxidase staining of lung tissue sections to confirm the location of neutrophils in the vasculature and lung tissues (bottom). Tissue sections are from SH rats exposed to 6 hours of tobacco smoke per day for 3 days, 4 weeks or 12 weeks.
Figure 2.
Mean linear intercept is reported as a measurement of alveolar airspace enlargement within the lung parenchyma after 3 days, 4 weeks or 12 weeks of filtered air or tobacco smoke exposure.
Figure 3.
Tobacco smoke induced adhesion molecule expression.
Top) Representative pictures of immunohistochemical (IHC) staining of E-selectin, VCAM, and ICAM in the bronchial wall of SH rats exposed to filtered air or 3 days of tobacco smoke. Arrows indicate bronchial blood vessels. Bottom) IHC staining intensity of the adhesion molecules E-selectin, VCAM, and ICAM after 3 days of tobacco smoke as scored by blinded ranking. Br BV: bronchial blood vessel; Par BV: parenchymal blood vessel. Brackets indicate comparisons between filtered air exposure and tobacco smoke exposure. (Note: Adhesion molecules and chemokine staining scores were reranked putting them on a 1–12 scale. See methods).
Figure 4.
Tobacco smoke induced chemokine expression.
Top) Representative pictures of immunohistochemical (IHC) staining of MCP-1 and MIP-2 in the bronchial wall of SH rats exposed to filtered air or 3 days of tobacco smoke. Bottom) IHC staining intensity of the chemokines MCP-1 and MIP-2 after 3 days of tobacco smoke as scored by blinded ranking. Br BV: bronchial blood vessel; Br Epi: bronchial epithelial cells; Alv. Mac: alveolar macrophages; Br Mac: macrophages in the bronchial wall. Brackets indicate comparisons between filtered air exposure and tobacco smoke exposure. (Note: Adhesion molecules and chemokine staining scores were reranked putting them on a 1–12 scale. See methods).
Table 1.
Adhesion molecule and chemokine expression at specific locations correlate with leukocytes recovered from the BALF.
Table 2.
Neutrophil specific adhesion molecule and chemokine expression at specific locations correlate with neutrophils recovered from the BALF.
Figure 5.
Smoke increases neovasculization.
Bronchial blood vessels per mm airway lumen at 3 days, 4 weeks and 12 weeks smoke exposure.
Figure 6.
Leukocytes recovered from the BALF of SH rats after 3 days, 4 weeks, or 12 weeks of tobacco smoke exposure.
Total leukocytes, monocyte/macrophages neutrophils, and lymphocytesrecovered from the BALF after 3 days, 4 weeks, or 12 weeks of tobacco smoke exposure.
Figure 7.
Adhesion molecule and chemokine expression in and around the bronchial blood vessels following 3 days, 4 weeks, or 12 weeks of tobacco smoke exposure.
Top) Representative pictures of immunohistochemical staining of E-selectin in the bronchial wall of SH rats exposed to filtered air or tobacco smoke for 3 days, 4 weeks, or 12 weeks. Arrows indicate bronchial blood vessels. Bottom) IHC staining intensity of E-selectin, VCAM, ICAM, MCP-1, and MIP-2 after 3 days, 4 weeks, or 12 weeks of tobacco smoke as scored by blinded ranking. The difference from control staining is reported as mean ± SEM, where the mean control staining at each location is set to zero. * p value<0.05 vs. filtered air. Brackets indicate comparisons between 3 days, 4 weeks and 12 weeks of smoke exposure. (staining scores were reranked prior to analysis changing the scale, see methods).