Published ahead of print on March 23, 2004, doi:10.1165/rcmb.2003-0394OC
© 2004 American Thoracic Society DOI: 10.1165/rcmb.2003-0394OC Complement Factors C3a, C4a, and C5a in Chronic Obstructive Pulmonary Disease and AsthmaUniversity Clinic of Respiratory and Allergic Diseases, Golnik, Slovenia Address correspondence to: Address correspondence to: Mateja M. Marc, M.D., University Clinic of Respiratory and Allergic Diseases, Golnik 36, 4204 Golnik, Slovenia. E-mail: mateja.marc{at}klinika-golnik.si 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.
Abbreviations: bronchoalveolar lavage fluid, BALF • complement, C • chronic obstructive pulmonary disease, COPD • diffusion capacity of the lungs for carbon monoxide, DLCO • forced expiratory volume in 1 s, FEV1 • forced vital capacity, FVC • total number of nonsquamous cells, TNNC This article has been cited by other articles:
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