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Induced sputum of patients with chronic obstructive pulmonary disease (COPD) contains adhesion-promoting, therapy-sensitive factors

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Objective: The aim of this study was to investigate whether sputum of COPD patients before and after treatment with inhaled corticosteroids (IHC) or N-acetylcysteine (NAC) exerts any effect on the adhesion of isolated polymorphonuclear cells (PMNs) to cultured endothelial cells.¶Methods: A human endothelial cell line was grown to confluence before use in adhesion experiments. PMNs were obtained from normal, non-smoking volunteers and preincubated (30 min, 37°C) with diluted sputum sol obtained from COPD patients before the cells were put on the endothelial cells.¶Results: Basal adhesion of unstimulated PMNs after 30 min at 37°C in 5% CO2 was 15.9 ± 1.1% (mean ± SEM, n = 9). A significant enhancement of the adhesion to 33.0 ± 1.4% (n = 11, P < 0.0001) was observed with sputum obtained from COPD patients before treatment with IHC, and 34.6 ± 1.5% (n = 10, P<0.0001) before treatment with NAC. Administration of IHC for 8 weeks resulted in an adhesion of 27.7 ± 2.4%, which is an inhibition of 31% (n = 11, P<0.05). However, treatment for 8 weeks with NAC showed no change in the adhesion of stimulated PMNs. Long-term treatment with NAC showed a gradual decrease of adhesion (n = 9, P<0.05), whereas long-term treatment with IHC lead to an increase in adhesion (n = 10, P<0.02).¶Conclusions: These results indicate that factors locally produced in the airways of COPD patients may pro-mote adhesion of neutrophils to endothelium. They further suggest that glucocorticoids may only have a short-term transient effect on adhesion, whereas NAC showed effects on the adhesion after administration for longer periods.¶

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Received 20 October 1998; returned for revision 15 December 1998; accepted by I. Ahnfelt-Rønne 14 September 1999

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van Overveld, F., Vermeire, P. & De Backer, W. Induced sputum of patients with chronic obstructive pulmonary disease (COPD) contains adhesion-promoting, therapy-sensitive factors. Inflamm. res. 49, 8–13 (2000). https://doi.org/10.1007/PL00000203

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  • DOI: https://doi.org/10.1007/PL00000203

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