Abstract
(1) Background: Progression of chronic obstructive pulmonary disease (COPD) leads to irreversible lung damage and inflammatory responses; however, biomarker discovery for monitoring of COPD progression remains challenging. (2) Methods: This study evaluated the metabolic mechanisms and potential biomarkers of COPD through the integrated analysis and receiver operating characteristic (ROC) analysis of metabolic changes in lung, plasma, and urine, and changes in morphological characteristics and pulmonary function in a model of PPE/LPS-induced COPD exacerbation. (3) Results: Metabolic changes in the lungs were evaluated as metabolic reprogramming to counteract the changes caused by the onset of COPD. In plasma, several combinations of phenylalanine, 3-methylhistidine, and polyunsaturated fatty acids have been proposed as potential biomarkers; the α-aminobutyric acid/histidine ratio has also been reported, which is a novel candidate biomarker for COPD. In urine, a combination of succinic acid, isocitric acid, and pyruvic acid has been proposed as a potential biomarker. (4) Conclusions: This study proposed potential biomarkers in plasma and urine that reflect altered lung metabolism in COPD, concurrently with the evaluation of the COPD exacerbation model induced by PPE plus LPS administration. Therefore, understanding these integrative mechanisms provides new insights into the diagnosis, treatment, and severity assessment of COPD.
Highlights
Chronic obstructive pulmonary disease (COPD) is a slowly developing respiratory disease that is accompanied by irreversible emphysema with chronic airway inflammation, mucus hypersecretion [1], and airway remodeling, and is one of the growing causes of death [2]
The vehicle control 2 (VC2) and COPD2 groups showed a significant increase in functional residual capacity (FRC), total lung capacity (TLC), forced vital capacity (FVC) (Figure S2a–c), and a decrease in the FEV 100/FVC (Figure S2d), when compared with the vehicle control 1 (VC1) and COPD1 groups
This study was a metabolomic study on the lungs, plasma, and urine in a porcine pancreatic elastase (PPE)/LPSinduced COPD exacerbation model
Summary
Chronic obstructive pulmonary disease (COPD) is a slowly developing respiratory disease that is accompanied by irreversible emphysema with chronic airway inflammation, mucus hypersecretion [1], and airway remodeling, and is one of the growing causes of death [2]. The main causes of COPD include cigarette smoke (CS), air pollution, fine dust, and exposure to various inducers in the workplace environment [3]. Studies are currently being conducted on various animal models to understand the biochemical mechanism of COPD [9]. The common methods of COPD induction in mice include exposure to CS or a combination inducer of elastase and lipopolysaccharide (LPS). The CS mouse model has the advantage of being able to best reflect the clinical symptoms of COPD, the method for animal exposure has not yet been standardized. The model that uses the combination inducer, elastase and LPS, enables easy induction of the disease, while allowing control over the severity of the disease based on the dose of the inducer, but has the disadvantage of reflecting several, but not all, pathophysiological changes, depending on emphysema [9]. The design and selection of an appropriate animal model is critical and should be done based on the purpose of the study
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