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. 2017 Jun;187(6):1288–1300. doi: 10.1016/j.ajpath.2017.02.008

Figure 1.

Figure 1

Mmp28 is required for chronic inflammatory changes to cigarette smoke exposure at 6 months. After 6 months of cigarette smoke exposure (SM) or room air control (NS), wild-type (WT) and Mmp28−/− mouse lungs were lavaged, and the bronchoalveolar lavage (BAL) leukocyte populations analyzed by cytospin. A: In SM mice compared to NS controls matched by genotype, there is a significant increase in total alveolar macrophages, neutrophils, and lymphocytes in response to cigarette smoke exposure. However, the absence of Mmp28 is associated with significantly smaller smoke-induced increases in macrophages (0.7-fold of WT SM), neutrophils (0.2-fold of WT SM), and lymphocytes (0.3-fold of WT SM) in the alveolar compartment. B: Alveolar tissue area (Atis) and mean chord length (CL) were quantified, and Atis decreases and CL increases in WT SM versus NS but not in Mmp28−/− SM mice. C: Representative histology (hematoxylin and eosin staining) of WT SM and Mmp28−/− SM compared to room air controls demonstrating mild emphysematous changes in WT SM mice (asterisks indicate enlarged alveoli). n = 10 mice per genotype per group (A–C). ∗P < 0.05. Scale bar = 500 μm (C).