Topical Area: Dietary Bioactive Components
Pulmonary emphysema characterized by loss of alveolar integrity is caused by damage to the alveoli as a result of prolonged exposure to cigarette smoke, inhaled irritants, air pollution and fine dust. Emphysema entails pulmonary inflammation of the lungs, narrowing of the small airways, and destruction of the lung tissues. Our previous study found that dry-yeast extracts inhibited eosinophilia and mucus overproduction in a murine model of asthma. The current study examined whether dry-yeast extracts ameliorated pulmonary emphysema in mice evoked by cigarette smoke.
Emphysema was induced by exposure of BALB/c mice to cigarette smoke for 30 min, five days a week for eight weeks. Mice were orally administrated with 50-200 mg/kg for 8 weeks. In the in vitro studies employing alveolar epithelial A549 cells 2 μg/ml lipopolysaccharide (LPS) was loaded in the absence and presence of 10-100 µg/ml dry-yeast extracts.
Oral supplementation of dry-yeast extracts reduced the influx of inflammatory cells such as neutrophils and eosinophils in lung promoted by cigarette smoke. H&E staining revealed that alveoli emphysema was evident in cigarette smoke-exposed lung, which was ameliorated by treating dry-yeast extracts to mice. Dry-yeast extract improved the apoptotic bax/antiapoptotic bcl-2 ratio of lung tissues damaged by cigarette smoke. In addition, the immunohistochemical analysis employing anti-MMP12 confirmed that dry-yeast extracts inhibited apoptotic damage of alveoli subjected to cigarette smoke. In lung tissues dry-yeast extracts attenuated the induction of cigarette smoke-promoted inducible cyclooxygenase-2, a key mediator of inflammatory pathways. In A549 cells exposed to LPS, dry-yeast extract attenuated alveolar inflammation.
These results demonstrated that dry-yeast extracts inhibited pulmonary inflammation leading to emphysema in small airways and alveoli exposed to cigarette smoke. Therefore, dry-yeast extracts may be a promising agent treating progressive pulmonary disorders including chronic obstructive pulmonary disease.
Funding Sources : This work (Grants No. C0501612) was supported by project for Cooperative R&D between Industry, Academy, and Research Institute funded Korea Ministry of SMEs and Startups in 20.