Synthesis and anti-inflammatory effect of lipoxins in human airway epithelial cells
| Autor: | Delphine Gras, Isabelle Vachier, Pascal Chanez, Brigitte Mainprice, Caroline Bonnans, C. Chavis, Philippe Godard |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
medicine.drug_class
Blotting Western Inflammation Bronchi Respiratory Mucosa Biology chemistry.chemical_compound Hydroxyeicosatetraenoic Acids medicine Humans Interleukin 8 Receptors Lipoxin Receptor Autocrine signalling Cells Cultured Chromatography High Pressure Liquid Pharmacology Lipoxin Tumor Necrosis Factor-alpha Immunochemistry Anti-Inflammatory Agents Non-Steroidal Interleukin-8 Epithelial Cells General Medicine Receptor antagonist Molecular biology Receptors Formyl Peptide Epithelium Lipoxins medicine.anatomical_structure chemistry Immunology Tumor necrosis factor alpha medicine.symptom |
| Zdroj: | Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 61(5) |
| ISSN: | 0753-3322 |
| Popis: | In this study, we investigated the synthesis of lipoxins (LXs) and their anti-inflammatory effects in different human airway epithelial cell culture models. After cell incubation with exogenous 5(S),6(R)-dihydroxy-7,9-trans-11,14-cis-eicosatetraenoic acid, LXA(4) was detected in supernatants of differentiated human bronchial epithelial cells by contrast to non-differentiated cells. Exogenous LXA(4) significantly inhibited tumor necrosis factor-alpha (TNF-alpha)-induced interleukin-8 (IL-8) release in the different epithelial cell types and the potency of inhibition was dependent of the accessibility of the specific LXA(4) receptor, formyl-peptide receptor like-1 (FPRL-1) expressed by all these cells. Immunohistochemistry analysis on human bronchial biopsies showed a high expression of FPRL-1 in the epithelium. Finally, an FPRL-1 receptor antagonist, boc-2 peptide reversed LXA(4) effect on IL-8 generation. Together, these findings indicate that differentiated human bronchial epithelium synthesizes LX in vivo which could have autocrine actions through its specific receptor FPRL-1 to promote resolution of airway inflammation. |
| Databáze: | OpenAIRE |
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