Studies of animal models have shown that the activation of the complement system could have a role in chronic obstructive pulmonary disease (COPD) and asthma by promoting inflammation and enhancing airway hyperresponsiveness. We sought to determine whether the levels of complement factors C3a, C4a, and C5a are elevated at the site of inflammation in patients with COPD and patients with asthma. We analyzed the induced sputum of seven patients with COPD, ten patients with asthma, and twelve healthy nonsmokers. The concentrations of anaphylatoxins in the induced sputum were measured by cytometric bead array. We found significantly increased C5a/C5a desArg concentrations in supernatants of the induced sputum of patients with COPD (P = 0.007) and those with asthma (P = 0.002) compared with the control group. In patients with COPD the C5a/C5a desArg concentrations were significantly negatively correlated with lung diffusion coefficient (r = -0.71, P = 0.035). There was no significant difference in C3a/C3a desArg or C4a/C4a desArg measurements between the three groups of subjects. These in vivo results propose the involvement of complement factor C5a in the pathogenesis of COPD and asthma.

The complement component C5a is a potent inflammatory peptide, which may be involved in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD). We analysed the induced sputum and plasma of 28 patients with stable COPD, 12 healthy smokers and 7 non‐smokers. In 13 of the patients with COPD, we also observed paired samples during acute exacerbation. The concentrations of C5a/C5a desArg and C3a/C3a desArg were measured using cytometric bead array. Both C5a and C3a concentrations in induced sputum of stable patients with COPD were significantly increased compared to the control groups of healthy smokers and non‐smokers. In addition, there was a significant elevation in C5a values in exacerbation of COPD that was independent from the airway C3a levels. Airway C5a levels were negatively correlated with forced expiratory volume in first second (FEV1)% predicted and diffusing capacity of the lung (TLCO). Plasma C5a concentrations in patients with COPD were significantly higher than in healthy smokers, but no further significant systemic C5a elevation was detected with acute exacerbation of COPD. There was no important difference in local or systemic C5a concentrations between healthy smokers and non‐smokers. These in vivo results clearly show that local and systemic C5a concentrations in COPD are elevated, and that the local, in contrast to systemic, C5a concentrations additionally increase in the acute exacerbation of COPD. It seems that the cigarette smoke is not related to C5a increase. The elevated local and systemic C5a levels, and additional individual local C5a increase during the exacerbation support the importance of C5a in COPD.

Angiogenesis is a prominent feature of structural tissue remodelling that occurs in chronic airway diseases, including chronic obstructive pulmonary disease (COPD). The aim of this study was to evaluate the airway levels of VEGF, angiogenin, IL‐8 and TNF‐α in patients with COPD during the stable phase and during acute exacerbation of the disease. We analysed induced sputum samples from 28 patients with COPD. Thirteen of these patients were followed up and second samples of sputum were obtained during acute exacerbation of the disease. The two control groups consisted of 12 healthy smokers and seven healthy non‐smokers, all with normal lung function tests. Concentrations of VEGF, angiogenin, IL‐8, TNF‐α and bFGF were measured by cytometric bead array. In the induced sputum of patients with stable COPD, concentrations of VEGF (P < 0.001, P = 0.02), angiogenin (P < 0.0001, P < 0.0001), IL‐8 (P < 0.0001, P = 0.0021) and TNF‐α (P < 0.001, P = 0.03) were significantly elevated in comparison with healthy smokers and non‐smokers. No additional elevation of angiogenic factors was demonstrated at the time of exacerbation. There was a significant negative correlation between FEV1 and VEGF (P < 0.05, r = −0.38), angiogenin (P < 0.0001, r = −0.68) and IL‐8 (P < 0.001, r = −0.54) among smokers (smoking COPD patients and healthy smokers). No significant differences were observed between groups of healthy smokers and non‐smokers. These results showed increased airway angiogenesis in patients with COPD. Moreover, VEGF, IL‐8 and angiogenin negatively correlated with pulmonary function, which suggests their important role in COPD airway remodelling. However, no additional angiogenic activation was found during exacerbation of COPD.

Cytotoxic CD8+ T cells have been suggested to be key players in the pathogenesis of chronic obstructive pulmonary disease (COPD). We wanted to investigate the phenotype of lung tissue T lymphocytes (LTL) and tumour‐infiltrating T lymphocytes (TIL) in smokers with peripheral non‐small cell lung carcinoma (NSCLC) with moderate/severe versus mild COPD. Lung tissue and tumour samples were obtained from patients with moderate/severe stage of COPD (n = 10) and from patients with mild stage of COPD (n = 7) at lung resection for a solitary peripheral NSCLC, processed and analysed by flow cytometry. The flow‐cytometric results showed that lung tissue T cells, regardless of the severity of COPD, were mostly of the activated phenotype, expressed the CXCR3 chemokine receptor characteristic of type 1 T cells, and did neither significantly differ in the expression of activation markers (CD69, CD25 and HLA‐DR), differentiation markers (CD27 and CD28) and chemokine receptors (CXCR3 and CCR4) between the selected groups, nor showed any significant correlation with lung function measured as forced expiratory volume in 1 s (FEV1) or TLCO. Compared with LTL, a significantly greater proportion of TIL expressed the activation markers CD69 and CD25, but a lower proportion showed a fully differentiated CD27−28− phenotype. We conclude that lung LTL patterns are similar in NSCLC patients with moderate/severe or mild stages of COPD, and are not significantly related to lung function. LTL and TIL possess different phenotype characteristics. The majority of tumour tissue T cells are activated, but it seems that their process of differentiation is incomplete.