Severe persistent asthma and chronic obstructive pulmonary disease (COPD) are associated with neutrophil influx into the airways. It is not clear whether neutrophil chemotaxis is influenced by beta(2)-agonists and glucocorticoids, drugs commonly used in treatment of asthma and COPD. The effect of a long-acting beta(2)-agonist (formoterol), and a glucocorticosteroid (budesonide) on chemokine/cytokine release (CXCL8, CXCL1, IL-6), regulation of chemokine receptors (CXCR1, CXCR2), and migration were assessed in neutrophils from 10 non-allergic, healthy donors. Formoterol enhanced and budesonide inhibited IL-6, CXCL8 and CXCL1 release from LPS-stimulated neutrophils. Formoterol up-regulated both CXCR1 and CXCR2 expression, whereas budesonide up-regulated the expression of CXCR2 only. Despite the effects on chemokine release and drug-induced up-regulation of CXCR1 and CXCR2, no influence on neutrophil chemotaxis could be demonstrated. We conclude that a beta(2)-agonist and a glucocorticoid, commonly used in the treatment of obstructive lung diseases, influence chemokine release and receptor sensitivity but the functional consequences of these findings remain unclear.
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