Effect of formoterol and budesonide on chemokine release,chemokine receptor expression and chemotaxis in human neutrophils |
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| Authors: | Karin Strandberg Kristin Blidberg Karin Sahlander Lena Palmberg Kjell Larsson |
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| Affiliation: | 1. Department of Toxicology, Faculty of Pharmacy, Yeditepe University, Kayisdagi, Istanbul, Turkey;2. Divisions of Biological Chemistry, Biocenter, Medical University, Innsbruck, Austria;3. Medical Biochemistry, Biocenter, Medical University, Innsbruck, Austria;4. Department of Pharmacognosy, Faculty of Pharmacy, Yeditepe University, Kayisdagi, Istanbul, Turkey;5. Central Institute of Blood Transfusion and Immunology, University Clinics, Innsbruck, Austria |
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| Abstract: | 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 β2-agonists and glucocorticoids, drugs commonly used in treatment of asthma and COPD. The effect of a long-acting β2-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 β2-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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