BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) have increased numbers of neutrophils and macrophages in their lungs. Growth related oncogene-alpha (GROalpha) 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 GROalpha 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 GROalpha 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) GROalpha and MCP-1 levels were significantly increased in sputum from patients with COPD compared with non-smokers and healthy smokers (GROalpha: 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 GROalpha and MCP-1 levels in sputum and forced expiratory volume in 1 second (FEV(1)) % predicted (GROalpha: r=-0.5, p<0.001; MCP-1: r=-0.5, p<0.001), together with significant positive correlations between GROalpha and MCP-1 and neutrophil numbers in sputum (GROalpha: r=0.6, p<0.001; MCP-1: r=0.4, p<0.01). CONCLUSION: These results suggest that GROalpha and MCP-1 are involved in the migration of inflammatory cells, thus contributing to the inflammatory load associated with COPD.
BACKGROUND:Patients with chronic obstructive pulmonary disease (COPD) have increased numbers of neutrophils and macrophages in their lungs. Growth related oncogene-alpha (GROalpha) 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 GROalpha 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 GROalpha 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) GROalpha and MCP-1 levels were significantly increased in sputum from patients with COPD compared with non-smokers and healthy smokers (GROalpha: 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 GROalpha and MCP-1 levels in sputum and forced expiratory volume in 1 second (FEV(1)) % predicted (GROalpha: r=-0.5, p<0.001; MCP-1: r=-0.5, p<0.001), together with significant positive correlations between GROalpha and MCP-1 and neutrophil numbers in sputum (GROalpha: r=0.6, p<0.001; MCP-1: r=0.4, p<0.01). CONCLUSION: These results suggest that GROalpha and MCP-1 are involved in the migration of inflammatory cells, thus contributing to the inflammatory load associated with COPD.
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