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

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

From: A disintegrin and metalloproteinase domain-15 deficiency leads to exaggerated cigarette smoke-induced chronic obstructive pulmonary disease (COPD)-like disease in mice

Fig. 5

a–c Four groups of Adam15 BM chimeric mice (WT BM transplanted into WT recipients [WT WT], Adam15−/− BM transplanted into WT recipients [KO WT], WT BM transplanted into Adam15−/− recipients [WT KO], and Adam15−/− BM transplanted 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 14–19 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. 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. 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.

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