FIG 6.
Depletion of pulmonary macrophages suppresses the development of experimental COPD. A–E, WT BALB/c mice were exposed to cigarette smoke or normal air for 8 weeks. These two groups of mice also were treated with either liposome encapsulated clodronate or empty liposomes (Sham) 3 times/week for the duration of the experiment commencing on the 1st day of smoking. Relative to smoke-exposed macrophage-sufficient mice, smoke-exposed macrophage-depleted mice had reduced (A) airway epithelium thickening; and (B) alveolar enlargement; and altered lung function; increased (C) transpulmonary and (D) increased airway-specific resistance (RI), and (E) reduced dynamic compliance (Cdyn). The smoke-exposed macrophage-depleted mice had no alveolar enlargement or changes in lung function compared to non-smoke exposed control mice. Data are means±SEM of 6–8 mice/group, ## P<0.01, ### P<0.001 compared to mice that breathed normal air, * P<0.05, ** P<0.01 *** P<0.001 compared to other groups indicated.