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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 3: Deficiency of Adam15 in mice increases CS-induced lung inflammation.

Figure 3:

Wild-type (WT) and Adam15−/− mice were exposed to air or CS for 1 month (Mo), 3 months or 6 months. Absolute numbers of all leukocytes (A), macrophages (B), and lymphocytes (C) were counted in bronchoalveolar lavage (BAL) samples. Data are mean ± SEM; n = 12-14 mice exposed to air and 6-11 mice exposed to CS. Data were analyzed using a One-Way ANOVA followed by pair-wise testing with two-tailed Student’s t-tests. *, P ≤ 0.005 versus the same genotype exposed to air or the group indicated. In D-H, WT and Adam15−/− mice were exposed to air or CS for 1 or 3 months, lungs were enzymatically digested, and leukocytes were immunostained for markers of lymphocyte subsets including CD4+ lymphocytes (D), CD8+ lymphocytes (E), CD3-positive NKT cells (F), Tregs (G), and B cells (H). Lymphocyte subsets were quantified using flow cytometry. Data are mean ± SD; n = 5 mice exposed to air and 8-9 mice exposed to CS. Data were analyzed using a One-Way ANOVA followed by pair-wise testing with two-tailed Student’s t-tests. *, P < 0.05 air-exposed mice belonging to the same genotype or the group indicated.