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. Author manuscript; available in PMC: 2021 Sep 7.
Published in final edited form as: Mucosal Immunol. 2020 Jul 20;14(2):342–356. doi: 10.1038/s41385-020-0325-3

Figure 5: Deficiency of Adam15 in bone marrow (BM)-derived leukocytes drives the exaggerated COPD-like disease detected in CS-exposed Adam15−/− mice.

Figure 5:

In A-C, 4 groups of Adam15 BM chimeric mice (WT BM into WT recipients [WT WT], Adam15−/− BM into WT recipients [KO WT], WT BM into Adam15−/− recipients [WT KO], and Adam15−/− BM into Adam15−/− recipients [KO KO]) were exposed to air or CS for 6 months. Panel A shows the mean alveolar chord lengths measured in the CS-exposed mice. The mean chord length in air-exposed mice was 14 to 19 μm in all groups (data not shown). Data are mean ± SEM; n = 4-6 mice/group. Data were analyzed using a One-Way ANOVA followed by pair-wise testing with two-tailed Student’s t-tests. *, P < 0.05 versus the group indicated. In B, the thickness of the ECM protein layer deposited around small airways was quantified in microns, as described in Methods. Data are mean ± SEM; n = 5-8 mice/group. Data were analyzed using a One-Way ANOVA followed by pair-wise testing with two-tailed Student’s t-tests. *, P ≤ 0.022 versus the group indicated. In C, the number of alveolar macrophages in lung sections normalized to alveolar wall area was measured, as described in the Methods. Data are mean ± SEM; n = 5-6 mice/group. Data were analyzed using a One-Way ANOVA followed by pair-wise testing with two-tailed Student’s t-tests. *, P < 0.05 versus the group indicated.