Metabolic Syndrome as a Factor Affecting Systemic Inflammation in Patients with Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a systemic disease which may be associated with other comorbidities. The aim of the study was to estimate the incidence of metabolic syndrome (MS) in COPD patients and to assess its impact on systemic inflammation and lung function. MS was diagnosed in accordance with the recommendations of the Polish Forum for the Prevention of Cardiovascular Diseases. The study group consisted of 267 patients with stable COPD in all stages of severity. All patients underwent spirometry with bronchial reversibility testing and 6 min walk test (6MWT). The following blood tests were evaluated: lipid profile, glucose and C-reactive protein as well as serum concentration of IL-6, leptin, adiponectin, and endothelin. MS was diagnosed in 93 patients (35.8%). No differences were observed in the incidence of MS in relation to airflow limitation severity (mild; moderate; severe and very severe: 38.9; 36.3; 35.2 and 25.0%, respectively). FEV1 (% predicted), FVC (% predicted), 6MWT distance (6MWD), age, and the number of pack-years were similar in patients with and without MS. MS was more frequent in males than females (38.7 vs. 28.4%, p > 0.05). Serum concentrations of IL-6, endothelin, leptin, and CRP were higher in the MS group, contrary to adiponectin concentration which was lower (p < 0.01). MS was more frequent in male COPD patients, but there were no differences in its frequency between patients with different severity of airflow limitation. We conclude that MS, as a comorbidity, occurs in all COPD stages and affects systemic inflammation. MS incidence does not depend on COPD severity.

Acute Response to Cigarette Smoking Assessed in Exhaled Breath Condensate in Patients with Chronic Obstructive Pulmonary Disease and Healthy Smokers.

The effect of acute exposure to cigarette smoke (CS) on the respiratory system has been less extensively studied than the long term effects of smoking. The aim of the present study was to evaluate the acute response to CS in smokers suffering from chronic obstructive pulmonary disease (COPD) and in healthy smokers. Nineteen stable COPD patients and 19 young healthy smokers were enrolled. Tumor necrosis factor alpha (TNF-α), IL-1ß, and malondialdehyde (MDA) were measured in exhaled breath condensate (EBC) before and 60 min after smoking a cigarette. When pre- and post-CS levels of the evaluated biomarkers were compared, no differences were found in either group. However, the post-CS MDA was significantly greater in healthy smokers than that in COPD patients; 20.41 vs. 16.81 nmol/L, p = 0.01, respectively. Post-CS TNF-α correlated inversely with FEV1/FVC in healthy smokers. We conclude that CS does not acutely increase the EBC concentration of the inflammatory markers either in COPD patients or healthy smokers. The short term CS-induced oxidative stress is higher in young smokers than in COPD patients, which what may indicate a higher susceptibility to CS content of the former.

Comparison of cellular and biochemical markers of airway inflammation in patients with mild-to-moderate asthma and chronic obstructive pulmonary disease: an induced sputum and bronchoalveolar lavage fluid study.

Although the clinical pictures of asthma and chronic obstructive pulmonary disease (COPD) may be similar, the pathogenesis differs in many aspects. The aim of the present study was to compare the cellular and biochemical features of airway inflammation in patients with asthma and COPD. The study was conducted in 22 patients with asthma (M/F 12/10, mean age 36 +/-14 years) and 17 patients with COPD (M/F 10/7, mean age 57 +/-11 years). Each patient underwent sputum induction followed by bronchoscopy, and bronchoalveolar lavage. Total and differential cell counts and the concentration of interleukin-8 (IL-8) and myeloperoxidase (MPO) were measured in induced sputum (IS) and BALF. We found no significant differences in the total and differential cell counts in IS between asthma and COPD patients. However, COPD patients showed an increased total macrophage count in BALF compared with asthma patients. The relative eosinophil count in BALF was significantly higher in patients with asthma vs. COPD. The concentration of IL-8 in IS and BALF was significantly higher in patients with COPD vs. asthma patients. The BALF concentration of MPO was significantly higher in patients with COPD compared with asthma patients. We conclude that the comparison of cellular composition and the concentration of inflammatory mediators in IS does not differentiate between asthma and COPD. The evaluation of BALF reveals more differences in the cellular and biochemical features of airways inflammation in patients with asthma and COPD than that of IS.

Effects of the phosphodiestrase-4 inhibitor rolipram on lung resistance and inflammatory reaction in experimental asthma.

The aim of this study was to evaluate the influence of pretreatment with the phosphodiesterase-4 inhibitor rolipram on pulmonary resistance, influx of inflammatory cells, and histamine concentration in bronchoalveolar lavage fluid (BALF) during an experimental asthmatic reaction induced in ovalbumin (OA)-sensitized guinea pigs, challenged with OA inhalation. The experiment was performed in three groups of guinea pigs: two experimental groups, pretreated with rolipram or dexamethasone, and a control group without any pretreatment. Lung resistance (LR) was continuously recorded under suppression of spontaneous breathing during early asthmatic reaction. BALF was obtained before and at three time points up to 24 hr after the challenge. In the untreated, control animals a transient, significant increase in neutrophils, total and CD4+ lymphocytes, macrophages, eosinophils, and in histamine concentration in BALF was noted. Pretreatment with rolipram significantly reduced LR, eosinophils infiltration, and histamine release into the bronchoalveolar space during the early asthmatic reaction. These effects were generally comparable with those of dexamethasone, except that dexamethasone also reduced the influx of neutrophils into BALF.