Dried Yeast Extracts Curtails Pulmonary Oxidative Stress, Inflammation and Tissue Destruction in a Model of Experimental Emphysema.

Yun-Ho Kim,Soo-Il Kim,Young-Hee Kang,Su Oh,Dong Kim,Kyung-Hee Kim,Eun-Jung Lee,Min-Kyung Kang,Hyeongjoo Oh,Yean-Jung Choi,Sang-Jae Park

doi:10.3390/antiox8090349

Abstract

Pulmonary emphysema is characterized by a loss of alveolar integrity due to prolonged cigarette smoking and inhaled irritants. Dried yeast extracts (YE) are employed as food additives, savory flavorings, or creation of umami taste sensations. Despite being rich in nutrition, their application as nutraceuticals and functional foods is not investigated much and little is known about the inhibition of pulmonary emphysema. This study examined whether YE ameliorated pulmonary emphysema in mice is evoked by cigarette smoke (CS) and ovalbumin (OVA). Mice were orally administrated with 25–100 mg/kg YE for 8 weeks. Alveolar epithelial A549 cells exposed to lipopolysaccharide or CS extracts (CSE) were supplemented with 10–100 µg/mL YE. Oral YE administration reduced bronchoalveolar lavage fluid leukocytosis in CS-/OVA-exposed mice. YE reduced induction of inflammatory mediators and MMP-12, and diminished reactive oxygen species production and emphysematous alterations in CS-challenged airways. The YE treatment blunted bax/bcl-2 ratio and activation of p53 and caspases in CS-exposed lungs. Apoptotic death was dampened in CSE-loaded YE-supplemented A549 cells. YE curtailed tissue levels of MMP-12 in inflammatory OVA-exposed lungs. YE abrogated the secretion of TNF-α and MCP-1 through blocking NF-κB signaling in endotoxin-loaded A549 cells. Thus, the antioxidant YE may therapeutically ameliorate oxidative stress and inflammatory tissue destruction in emphysematous diseases.

Highlights

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease with the resultant airflow obstruction from the lungs [1,2]
This study examined whether yeast extracts (YE) abrogated airway inflammation and apoptotic emphysema in cigarette smoke (CS)- and OVA-challenged mouse models
This study examined how YE inhibited CS-evoked inflammation in mouse airways

Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease with the resultant airflow obstruction from the lungs [1,2]. Chronic bronchitis and emphysema are the most common disorders responsible for COPD, being caused by long-term exposure to irritating noxious gases, most often from cigarette smoke (CS) [5]. Chronic bronchitis is inflammation of the lining of the bronchial tubes, and emphysema is a condition in which the alveoli of the lungs are destroyed [6]. Pathological alterations in bronchioles and alveoli lead to a loss of alveolar integrity through activating aberrant inflammatory pathways [5]. Bronchiolar and alveolar epithelial cells can display direct immune and anti-inflammatory responses against lung tissue damage [6,7]

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