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Procaterol inhibits IL-1beta- and TNF-alpha-mediated epithelial cell eosinophil chemotactic activity
S Koyama1, E Sato, T Masubuchi
1The First Dept of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Abstract:
Theophylline inhibits eosinophilic infiltration into the bronchial wall. It is unknown whether this is mediated by a cyclic adenosine monophosphate (c-AMP)-dependent reduction in eosinophil chemotactic activity (ECA) from bronchial epithelial cells (BEC). Therefore the effect of a beta2-agonist, procaterol and theophylline on the release of ECA from a BEC line, BEAS-2B was evaluated in response to interleukin (IL)-1beta and tumour necrosis factor-alpha (TNF-alpha). ECA was assessed using a blind-well chemotactic chamber, and the release and gene expression of cytokines were evaluated by means of enzyme-linked immunosorbent assay and reverse transcriptase polymerase chain reaction. IL-1beta and TNF-alpha stimulated the release of ECA from BEAS-2B cells in a dose- and time-dependent manner. Procaterol and theophylline directly inhibited eosinophil migration to IL-1beta and TNF-alpha-conditioned medium. The pretreatment of BEAS-2B cells with the same concentrations of procaterol inhibited the release of ECA in a dose-dependent fashion. Anti-IL-8, anti-regulated on activation, normal T-cell expressed and secreted (RANTES), and anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) inhibited ECA. Procaterol inhibited the release of RANTES, GM-CSF and IL-8 in a dose-dependent fashion. The effect of theophylline was less potent. Procaterol augmented cAMP levels in BEAS-2B cells in a time- and dose-dependent manner. The expression of IL-8, RANTES, and GM-CSF messenger ribonucleic acid was not inhibited by procaterol and theophylline. These data indicate that procaterol and theophylline may directly inhibit eosinophil migration and that procaterol may further inhibit the release of eosinophil chemotactic activity from BEAS-2B cells via a cyclic adenosine monophosphate-dependent mechanism. This warrants further studies on the involvement of bronchial epithelial cells in the anti-inflammatory effects of procaterol and theophylline in patients with asthma.
Insights
Theophylline and procaterol inhibit eosinophil migration to the airways. Procaterol also reduces eosinophil chemotactic activity release from bronchial cells via a cyclic adenosine monophosphate-dependent pathway.
Area of Science:
- Pulmonology
- Immunology
- Pharmacology
Background:
- Theophylline reduces eosinophilic infiltration in asthma.
- The mechanism involving cyclic adenosine monophosphate (cAMP) and bronchial epithelial cells (BECs) is unclear.
Purpose of the Study:
- To investigate the effects of procaterol and theophylline on eosinophil chemotactic activity (ECA) release from BEAS-2B cells.
- To determine if these effects are mediated by a cAMP-dependent pathway.
Main Methods:
- BEAS-2B cells were stimulated with interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha).
- Eosinophil migration was assessed using a chemotactic chamber.
- Cytokine release and gene expression were measured via ELISA and RT-PCR.
- cAMP levels were quantified.
Main Results:
- IL-1beta and TNF-alpha increased ECA release from BEAS-2B cells.
- Procaterol and theophylline directly inhibited eosinophil migration.
- Procaterol pretreatment reduced ECA release and inhibited IL-8, RANTES, and GM-CSF release.
- Procaterol increased cAMP levels in BEAS-2B cells.
- Theophylline showed less potent effects.
Conclusions:
- Procaterol and theophylline directly inhibit eosinophil migration.
- Procaterol inhibits ECA release from BECs via a cAMP-dependent mechanism.
- Further research is needed on BEC involvement in the anti-inflammatory effects of these drugs in asthma.
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