The major findings of this study can be summarized as follows: 1) Autophagic markers were increased in airway epithelium and lung tissues, and impairment of autophagy reduced the neutrophilic airway inflammation and mucus hyperproduction in the CS+Eln model; 2) treatment of an autophagic inhibitor 3-MA either during CS-initiated sensitization or elastin provocation significantly inhibited the bronchitis-like phenotypes in mice; 3) autophagy mediated MMP12 activation in macrophages during the sensitization played a pivotal role in this novel mouse model of COPD. This evidence concerns the gene ELN and bronchitis.