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. 2023 Mar 22;8(6):e130771. doi: 10.1172/jci.insight.130771

Figure 3. Treatment with rhCC16 limits the progression of CB-like disease in WT and Cc16–/– mice exposed for CS for up to 8 weeks.

Figure 3

In A, WT and Cc16–/– mice were exposed to air (5–8 mice/group) or CS (4 mice/group) for 3 weeks, which is sufficient to impair mucociliary clearance (MCC) in WT mice (16). Other cohorts of mice were exposed to CS for 3 weeks, and then thrice weekly treatment with rhCC16 (75 μg of rhCC16; 4–5 mice/group) or vehicle (3–8 mice/group) delivered by the i.n. route was initiated and continued during an additional 2 weeks of CS exposure. 99mTc-sc was instilled into the lungs of anesthetized mice, and the efficiency of 99mTc-sc clearance from lungs was measured using noninvasive, 3-dimensional μ-SPECT imaging. In B–D, WT and Cc16–/– mice were exposed to air (7 mice/group) or CS for 8 weeks (15–17 mice/group). CS-exposed mice were treated thrice weekly with rhCC16 (8 mice/group) or vehicle (7–9 mice/group) for the last 4 weeks of the 8-week CS exposures. The expression of Foxj1 (B), mucin 5ac (Muc5ac; C), and Muc5b (D) was measured in whole lung samples using reverse transcription quantitative real-time PCR (RT-qPCR). In A–D, boxes in the box plots show the medians and 25th and 75th percentiles, and the whiskers show the 10th and 90th percentiles. Data were analyzed using 1-way ANOVAs followed by pairwise testing with Mann-Whitney U tests. Asterisks indicate P < 0.05 vs. air-exposed mice belonging to the same genotype or the group indicated.