Abstract | BACKGROUND: The interaction between leukocytes and various parenchymal cells is the first step of inflammation. Therefore, the adhesion of eosinophils to lung fibroblasts is thought to be a crucial step in the inflammatory process of asthma. Procaterol, a beta(2)-selective full agonist, is currently prescribed for patients with asthma. In addition to its potent bronchodilatory action, the agonist has been reported to have anti-inflammatory actions. In this study, to examine whether procaterol can potentiate the anti-inflammatory action of glucocorticoids, the effect of procaterol on eosinophil adhesion to normal human lung fibroblasts (NHLF) was assessed in the presence and absence of budesonide, one of the most potent glucocorticoids. METHODS: RESULTS: Pretreatment with procaterol inhibited the adhesion of eosinophils to NHLF in a concentration-dependent manner, and shifted the concentration-response curve of budesonide to the left. Both procaterol and budesonide resulted in concentration-dependent inhibition of expression of ICAM-1 and VCAM-1 in NHLF, and an additive inhibitory effect was found when the agents were combined. CONCLUSIONS:
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Authors | Norihiro Yoshida, Masahiro Muraguchi, Masayuki Kamata, Katsumi Ikezono, Toyoki Mori |
Journal | International archives of allergy and immunology
(Int Arch Allergy Immunol)
Vol. 150
Issue 4
Pg. 352-8
( 2009)
ISSN: 1423-0097 [Electronic] Switzerland |
PMID | 19571567
(Publication Type: Journal Article)
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Copyright | Copyright 2009 S. Karger AG, Basel. |
Chemical References |
- Anti-Inflammatory Agents
- Chemokine CCL11
- Tumor Necrosis Factor-alpha
- Vascular Cell Adhesion Molecule-1
- Intercellular Adhesion Molecule-1
- Budesonide
- Procaterol
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Topics |
- Anti-Inflammatory Agents
(pharmacology)
- Asthma
(drug therapy, immunology, metabolism, pathology)
- Budesonide
(pharmacology)
- Cell Adhesion
(drug effects, immunology)
- Cell Line
- Chemokine CCL11
(metabolism)
- Dose-Response Relationship, Drug
- Drug Synergism
- Eosinophils
(drug effects, immunology, metabolism, pathology)
- Fibroblasts
(drug effects, immunology, metabolism, pathology)
- Humans
- Intercellular Adhesion Molecule-1
(genetics, immunology, metabolism)
- Lung
(pathology)
- Procaterol
(pharmacology)
- Tumor Necrosis Factor-alpha
(metabolism)
- Vascular Cell Adhesion Molecule-1
(genetics, immunology, metabolism)
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