Inflammation, Oxidative Stress and Systemic Effects in Mild Chronic Obstructive Pulmonary Disease

Abstract

Chronic obstructive pulmonary diseases (COPD) is a pulmonary disease characterized by systemic abnormalities. The aim of this study is to investigate inflammation and systemic effects in mild COPD. Twenty-seven mild stable smoking related COPD patients and 15 age-matched healthy subjects were enrolled in the study. IL-6, TNF-a and IL-4 in plasma, sputum and exhaled breath condensate were measured. We also measured exhaled nitric oxide (NO) and pH in sputum and in breath condensate. Moreover, fat-free mass, body mass index (BMI), respiratory muscle strength, plasma oxidative stress and C-reactive protein (CRP) were measured. Higher concentrations were found of CRP, of diacron reactive oxygen metabolites (DROMs) and ofIL-6, TNF-a and IL-4 either in plasma or in supernatant of induced sputum or in exhaled breath condensate of COPD subjects compared to healthy controls. Furthermore, higher concentrations were observed of exhaled NO and lower exhaled pH in breath condensate of COPD when compared with healthy subjects. In the group of COPD patients, the subjects with airway reversibility showed an increase of sputum eosinophils and exhaled NO, whereas the subjects without airway obstruction reversibility showed an increase in sputum neutrophils, TNF-a and IL-6. We also found a trend towards a decrease in fat-free mass and respiratory muscle strength in COPD compared to healthy subjects and a negative correlation between these systemic indices (fatfree mass, maximal inspiratory pressure, maximal expiratory pressure) and TNF-a concentrations in the blood, sputum and breath condensate. We conclude that mild COPD subjects present an increase in inflammatory markers in blood and in airways of similar pattern and furthermore, the neutrophilic pattern of airway inflammation observed in the group of COPD subjects without an airway obstruction reversibility makes it more likely that systemic features are present.Chronic obstructive pulmonary disease (COPD) is usually considered to be a pulmonary disease (1). However, recent studies have demonstrated several extra-pulmonary abnormalities, particularly in more severely affected patients, that suggest the necessity of a wider definition of this disease (2). Several systemic features have been described in COPD patients, including systemic inflammation and oxidative stress, skeletal muscle dysfunction (SMD), weight loss, atherosclerosis and osteoporosis (3-5).

Levels of leptin and IL-6 in lungs and blood are associated with the severity of chronic obstructive pulmonary disease in patients and rat models

“…Walter et al (29) showed that plasma IL-6 levels, together with age and smoking, are independent risk factors for reduced FEV1. Foschino et al (30) demonstrated that IL-6 expression levels in the airway epithelial cells of COPD patients in the acute exacerbation stage were higher compared with those in stable COPD and healthy control patients, and that IL-6 expression levels in stable COPD patients were significantly increased compared with those of healthy controls. These findings are consistent with those of the present study, with the exception that IL-6 levels in patients with stable COPD were only slightly higher compared with those in healthy controls.…”

Role of Vasoactive Intestinal Peptide in Hyperoxia-Induced Injury of Primary Type II Alveolar Epithelial Cells

“…However, pulmonary epithelial damage is the major drawback of hyperoxia exposure [9]. AECII as the epithelial stem cell plays an important role in the maintenance of the alveolar integrity.…”

Time course of cigarette smoke-induced changes of systemic inflammation and muscle structure

“…Thereby, glutamate is an important precursor for the first and rate-limiting step in the synthesis of reduced glutathione, one of the most important antioxidants in muscle (5). Reduced muscle glutathione levels often result in an antioxidant/oxidant imbalance, increasing the susceptibility of the muscle to oxidative stress and cell injury (18). However, current concepts assume that oxidative stress plays a relevant role in the generation of skeletal muscle abnormalities in COPD (5).…”