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. 2003 Dec;163(6):2329–2335. doi: 10.1016/S0002-9440(10)63589-4

Figure 2.

Figure 2.

Neutrophil elastase is involved in inflammatory cell recruitment in response cigarette smoke. A: Neutrophils that underwent transvascular migration to the alveolar space were quantified by bronchoalveolar lavage. Note, NE and MMP-12 did not affect recruitment in non-smoke-exposed mice (solid bars). However, NE but not MMP-12 is required for neutrophil migration in response to cigarette smoke (hatched bars). Statistically, there were more neutrophils in wild-type (WT) non-smoke-exposed (NS) versus smoke exposed (Sm)(P < 0.01), and in MMP-12−/− NS versus MMP-12−/− Sm (P < 0.01), but not NE−/− NS versus NE−/− Sm. However, NE Sm had significantly fewer neutrophils than WT Sm (P < 0.01). B: Tissue macrophage counts were assessed by immunhistochemical (mac-3) staining of mid-sagittal sections and equalized for alveolar tissue density. Note, cigarette smoke exposure increased macrophages in WT mice (WT NS versus WT Sm, P < 0.001) and NE−/− mice (NE−/− NS versus NE−/− Sm, P = 0.04), but not MMP-12−/− mice (MMP-12−/− NS versus MMP-12−/− Sm, P = 0.5). However, macrophage accumulation in response to cigarette smoke was inhibited 60% in NE−/− mice (WT Sm versus NE−/− Sm, P < 0.05), and 85% in MMP-12−/− mice (WT Sm versus MMP-12−/− Sm, P < 0.01). At least 10 mice were used for each group. Bars represent SE.