PT - JOURNAL ARTICLE AU - Traves, S L AU - Culpitt, S V AU - Russell, R E K AU - Barnes, P J AU - Donnelly, L E TI - Increased levels of the chemokines GROα and MCP-1 in sputum samples from patients with COPD AID - 10.1136/thorax.57.7.590 DP - 2002 Jul 01 TA - Thorax PG - 590--595 VI - 57 IP - 7 4099 - http://thorax.bmj.com/content/57/7/590.short 4100 - http://thorax.bmj.com/content/57/7/590.full SO - Thorax2002 Jul 01; 57 AB - Background: Patients with chronic obstructive pulmonary disease (COPD) have increased numbers of neutrophils and macrophages in their lungs. Growth related oncogene-α (GROα) attracts neutrophils, whereas monocyte chemoattractant protein-1 (MCP-1) attracts monocytes that can differentiate into macrophages. The aim of this study was to determine the concentration of GROα and MCP-1 in bronchoalveolar lavage (BAL) fluid and sputum from non-smokers, healthy smokers and patients with COPD, and to see if there was a correlation between the concentrations of these chemokines, lung function, and numbers of inflammatory cells. Methods: BAL fluid and sputum from non-smokers (n=32), healthy smokers (n=36), and patients with COPD (n=40) were analysed for the presence of GROα and MCP-1 using ELISA. Cells counts were performed on the samples and correlations between the concentrations of these chemokines, lung function, and inflammatory cells observed. Results: Median (SE) GROα and MCP-1 levels were significantly increased in sputum from patients with COPD compared with non-smokers and healthy smokers (GROα: 31 (11) v 2 (2) v 3 (0.8) ng/ml; MCP-1: 0.8 (0.4) v 0.2 (0.1) v 0.1 (0.04) ng/ml, p<0.05), but not in BAL fluid. There were significant negative correlations between both GROα and MCP-1 levels in sputum and forced expiratory volume in 1 second (FEV1) % predicted (GROα: r=–0.5, p<0.001; MCP-1: r=–0.5, p<0.001), together with significant positive correlations between GROα and MCP-1 and neutrophil numbers in sputum (GROα: r=0.6, p<0.001; MCP-1: r=0.4, p<0.01). Conclusion: These results suggest that GROα and MCP-1 are involved in the migration of inflammatory cells, thus contributing to the inflammatory load associated with COPD.