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BALB/c mice (female, 10 weeks; Emphysema, alongside chronic bronchitis, is the most common condition in chronic obstructive pulmonary disease (COPD), for which cigarette smoke (CS) is the most common causative factor.






We employed live animal imaging to monitor emphysema‐like development and the effects of interventional azithromycin treatment in CS‐exposed mice. Einfach Postleitzahl oder Ort eingeben und fündig werden! Half were cotreated with low‐dose azithromycin during weeks 7–12 (CS + Azi; 0.2 mg kg −1 day −1).
(a–c) Representative H&E‐stained lung sections at 12 weeks.

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(d) Mean linear intercept (Lm) values were taken as a measure of alveolar size and emphysematous changes.

Gastrointestinal, Hepatic and Pancreatic PhysiologyI have read and accept the Wiley Online Library Terms and Conditions of UseAzithromycin for prevention of exacerbations in COPDAlveolar wall apoptosis causes lung destruction and emphysematous changesCellular and molecular mechanisms of chronic obstructive pulmonary diseaseInflammatory mechanisms in patients with chronic obstructive pulmonary diseaseA new short‐term mouse model of chronic obstructive pulmonary disease identifies a role for mast cell tryptase in pathogenesisEvaluation of lung inflammation induced by intratracheal administration of LPS in mice: Comparison between MRI and histologyImprovements in lung function with nebulized revefenacin in the treatment of patients with moderate to very severe COPD: Results from two replicate phase III clinical trialsEffect of azithromycin on asthma exacerbations and quality of life in adults with persistent uncontrolled asthma (AMAZES): A randomised, double‐blind, placebo‐controlled trialAzithromycin increases phagocytosis of apoptotic bronchial epithelial cells by alveolar macrophagesAzithromycin improves macrophage phagocytic function and expression of mannose receptor in chronic obstructive pulmonary diseaseTherapeutic role for mannose‐binding lectin in cigarette smoke–induced lung inflammation?

Kruskal–Wallis analysis of percentage changes revealed no significant intercohort differences at the time points examined (Figure Significantly decreased average HU values in the lower lungs were observed in CS mice at week 12 [−399.5 HU (−408.2 – −394.5)] compared with both control mice [−384.9 HU (−390.1 – −373)] and CS + Azi mice [−377.3 HU (−384.2 – −370.2)] (Figure MRI examination of lung inflammation revealed a 27.28% increase in TEmphysema and increased inflammation are two components characteristic of the COPD phenotype.



Five µm sections were stained with H&E, then imaged at 20× objective resolution using a NanoZoomer 2.0‐HT (Hamamatsu Photonics, Japan), and viewed using NDP.view 2 software (Hamamatsu) for further analysis.Mean linear intercept (Lm) values advised alveolar size and the extent of emphysematous changes (Aoshiba, Yokohori, & Nagai, Micro‐CT images were acquired via the Skyscan 1,176 (Bruker Physik GmbH, Germany) at weeks 0, 6, 8, 10, and 12 using a 55 kV source voltage, 455 µA source current, 0.7° rotation step, 200 ms exposure, and 18 µm pixel size; physiological monitoring mode was synchronized to chest movement.

Data represent the average Lm based on the measurements taken from 3 lung sections per mouse; median ± range. Auch im Sputum werden hohe Konzentrationen erreicht.

The observed increase of approximately 20% is comparable with prior work in BALB/c and C57BL/6 mice, and reported to be indicative of emphysema in these animals (Beckett et al., Time‐course analysis of average CT values (HU) of the lower lung was statistically nonsignificant between cohorts until week 12; CS + Azi mice showed lung density recovery to control levels by this time point.

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