The Immunomodulatory Effect of Sevoflurane in Endotoxin-Injured Alveolar Epithelial Cells
| Autor: | Livia Reyes, Stephan Blumenthal, Dominik Suter, Christa Booy, Beatrice Beck-Schimmer, Donat R. Spahn, Birgit Roth Z'graggen |
|---|---|
| Přispěvatelé: | University of Zurich, Beck-Schimmer, B |
| Rok vydání: | 2007 |
| Předmět: |
Lipopolysaccharides
Methyl Ethers Chemokine Lipopolysaccharide Neutrophils Chemokine CXCL1 Chemokine CXCL2 610 Medicine & health Pharmacology Lung injury Epithelium Sevoflurane 10052 Institute of Physiology chemistry.chemical_compound Cell Adhesion Animals Medicine Macrophage Chemokine CCL4 Lung Chemokine CCL2 Anesthetics biology business.industry Monokines Monocyte Chemotaxis Macrophage Inflammatory Proteins Intercellular Adhesion Molecule-1 Rats Endotoxins Pulmonary Alveoli Anesthesiology and Pain Medicine medicine.anatomical_structure chemistry 10076 Center for Integrative Human Physiology Anesthetics Inhalation Anesthetic Immunology biology.protein 570 Life sciences 2703 Anesthesiology and Pain Medicine business Chemokines CXC medicine.drug |
| Zdroj: | Anesthesia & Analgesia. 104:638-645 |
| ISSN: | 0003-2999 |
| DOI: | 10.1213/01.ane.0000255046.06058.58 |
| Popis: | BACKGROUND: Endotoxin-induced lung injury is a useful experimental system for the characterization of immunopathologic mechanisms in acute lung injury. Although alveolar epithelial cells (AEC) are directly exposed to volatile anesthetics, there is limited information about the effect of anesthetics on these cells. In this study we investigated the effect of pretreatment with the inhaled anesthetic sevoflurane on lipopolysaccharide (LPS)-injured AEC. METHODS: AEC were incubated with 1.1 vol % sevoflurane for 0.5 h, followed by LPS stimulation for 5 h. Expression of monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1beta (MIP-1beta), macrophage inflammatory protein-2 (MIP-2), cytokine-induced neutrophil chemoattractant-1 (CINC-1), and intercellular adhesion molecule-1 (ICAM-1) was analyzed. In addition, functional tests were performed through chemotaxis and adherence assays to underline the biological relevance of the findings. RESULTS: Exposure of AEC to sevoflurane resulted in a 50% downregulation of MCP-1 protein in the sevoflurane-LPS group when compared with non-sevoflurane- LPS cells (P < 0.05). MIP-1beta concentration in LPS-stimulated cells decreased by 32% with sevoflurane (P < 0.05), MIP-2 by 29% (P < 0.05), and CINC-1 by 20% (P < 0.05). ICAM-1 protein expression was attenuated by 36% (P < 0.05). This inhibition caused substantial changes in the inflammatory response of neutrophils. 33% less chemotactic activity was seen in sevoflurane-treated LPS cells (P < 0.001) as well as 47% decreased adhesion of neutrophils to AEC (P < 0.001). CONCLUSIONS: This study shows that sevoflurane alters the LPS-induced inflammatory response, not only with respect to the expression pattern of inflammatory mediators, but also regarding the biological consequences with less accumulation of effector cells such as neutrophils. |
| Databáze: | OpenAIRE |
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