8-iso-prostaglandin-a2 and Pulmonary-Disease--Chronic-Obstructive

Topics: Analgesics; Animals; Anti-Inflammatory Agents; Asthma; Humans; Ion Channel Gating; Neurons; Pain; Peripheral Nervous System Diseases; Pulmonary Disease, Chronic Obstructive; Transient Receptor Potential Channels

Pulmonary hypertension (PH) is a common complication of chronic obstructive pulmonary disease (COPD). Although alveolar hypoxia is considered as a main cause of PH in COPD, structural and functional changes of pulmonary circulation are apparent at the initial stage of COPD. We hypothesized that an inflammatory response and oxidative stress might contribute to the formation of PH in COPD.. We measured the levels of interleukin-6 (IL-6) and 8-iso-prostaglandin (8-iso-PSG) in exhaled breath condensate (EBC) and serum in 40 patients with COPD only or in 45 patients with COPD combined with PH. Pulmonary arterial systolic pressure (PASP) was assessed by Doppler echocardiography and defined as PH when the value of systolic pressure was greater than 40 mmHg.. Compared with the COPD only group, the level of IL-6 in EBC was significantly increased in all 45 patients with COPD combined with PH ((8.27±2.14) ng/L vs. (4.95±1.19) ng/L, P < 0.01). The level of IL-6 in serum was also elevated in patients with COPD combined with PH compared with the COPD only group ((72.8±21.6) ng/L vs. (43.58±13.38) ng/L, P < 0.01). Similarly, we also observed a significant increase in the level of 8-iso-PSG in both EBC and serum in the COPD with PH group, compared with the COPD only group (EBC: (9.00±2.49) ng/L vs. (5.96±2.31) ng/L, P < 0.01 and serum: (41.87±9.75) ng/L vs. (27.79±11.09) ng/L, P < 0.01). Additionally, the value of PASP in the PH group was confirmed to be positively correlated with the increase in the levels of IL-6 and 8-iso-PSG in both EBC and serum (r = 0.477-0.589, P < 0.05).. The increase in the levels of IL-6 and 8-iso-PSG in EBC and serum correlates with the pathogenesis of PH in COPD.

Topics: Aged; Breath Tests; Female; Humans; Hypertension, Pulmonary; Interleukin-6; Male; Middle Aged; Prostaglandins A; Pulmonary Disease, Chronic Obstructive

Chronic obstructive pulmonary disease (COPD) patients have increased neutrophils and macrophages in their lungs, and inflammation of the airway is related to oxidative stress. This study assessed the levels of 8-isoprostane (an oxidative stress marker) and chemokines related to neutrophil and monocyte inflammation (growth-related oncogene alpha [GROalpha] and monocyte chemoattractant protein-1 [MCP-1]) in the airway of ex-smoking COPD patients by exhaled breath condensate (EBC) collection. Thirty-two (28 males) stable COPD patients (14 with FEV(1) 50% [Group 1], 18 with FEV(1) <50% predicted [Group 2]) and 18 non-smoking age and sex-matched controls were studied in this cross-sectional study. EBC was collected using the EcoScreen (Jaeger, Germany) during 10 min of tidal breathing with the nose clipped. Concentrations of 8-isoprostane, GROalpha and MCP-1 were measured by enzyme immunoassays. COPD patients had a higher concentration of 8-isoprostane than controls (COPD versus control, P<0.001; Group 1 versus Group 2, P=0.045). 8-isoprostane increased across the groups from normal, Group 1 to Group 2 (r=0.64, P<0.001). The median intraquartile range (IQR) levels in pg/ml for GROalpha were 45.3(44.5-46.5), 45.4(44.5-46.0), 46.0(45.6-47.3), whereas MCP-1 levels were 5.3(5.2-5.9), 6.2(5.4-6.9) and 5.7(5.5-6.4) in Group 1, Group 2 COPD and control subjects, respectively. GROalpha level was lower in COPD patients when compared to controls (P=0.01). MCP-1 level did not differ between COPD and the control group. 8-isoprostane level, but not GROalpha and MCP-1, in EBC was increased in COPD patients with poorer lung function. This suggests an increased oxidative stress in the airway in patients with more severe COPD.

Topics: Aged; Aged, 80 and over; Biomarkers; Breath Tests; Chemokine CCL2; Chemokine CXCL1; Chemokines, CXC; Cross-Sectional Studies; Female; Humans; Intercellular Signaling Peptides and Proteins; Male; Middle Aged; Oncogenes; Oxidative Stress; Prospective Studies; Prostaglandins A; Pulmonary Disease, Chronic Obstructive