PMID- 17312223 OWN - NLM STAT- MEDLINE DCOM- 20070327 LR - 20181201 IS - 1526-7598 (Electronic) IS - 0003-2999 (Linking) VI - 104 IP - 3 DP - 2007 Mar TI - The immunomodulatory effect of sevoflurane in endotoxin-injured alveolar epithelial cells. PG - 638-45 AB - 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. FAU - Suter, Dominik AU - Suter D AD - Institute of Anesthesiology, University of Zurich, Zurich, Switzerland. FAU - Spahn, Donat R AU - Spahn DR FAU - Blumenthal, Stephan AU - Blumenthal S FAU - Reyes, Livia AU - Reyes L FAU - Booy, Christa AU - Booy C FAU - Z'graggen, Birgit Roth AU - Z'graggen BR FAU - Beck-Schimmer, Beatrice AU - Beck-Schimmer B LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Anesth Analg JT - Anesthesia and analgesia JID - 1310650 RN - 0 (Anesthetics) RN - 0 (Anesthetics, Inhalation) RN - 0 (Ccl2 protein, rat) RN - 0 (Chemokine CCL2) RN - 0 (Chemokine CCL4) RN - 0 (Chemokine CXCL1) RN - 0 (Chemokine CXCL2) RN - 0 (Chemokines, CXC) RN - 0 (Cxcl1 protein, rat) RN - 0 (Endotoxins) RN - 0 (Lipopolysaccharides) RN - 0 (Macrophage Inflammatory Proteins) RN - 0 (Methyl Ethers) RN - 0 (Monokines) RN - 126547-89-5 (Intercellular Adhesion Molecule-1) RN - 38LVP0K73A (Sevoflurane) SB - IM MH - Anesthetics/pharmacology MH - Anesthetics, Inhalation/pharmacology MH - Animals MH - Cell Adhesion MH - Chemokine CCL2/metabolism MH - Chemokine CCL4 MH - Chemokine CXCL1 MH - Chemokine CXCL2 MH - Chemokines, CXC/metabolism MH - Endotoxins/*pharmacology MH - Epithelium/*drug effects MH - Intercellular Adhesion Molecule-1/metabolism MH - Lipopolysaccharides/metabolism/pharmacology MH - Lung/cytology MH - Macrophage Inflammatory Proteins/metabolism MH - Methyl Ethers/*pharmacology MH - Monokines/metabolism MH - Neutrophils/drug effects/metabolism MH - Pulmonary Alveoli/*drug effects MH - Rats MH - Sevoflurane EDAT- 2007/02/22 09:00 MHDA- 2007/03/28 09:00 CRDT- 2007/02/22 09:00 PHST- 2007/02/22 09:00 [pubmed] PHST- 2007/03/28 09:00 [medline] PHST- 2007/02/22 09:00 [entrez] AID - 104/3/638 [pii] AID - 10.1213/01.ane.0000255046.06058.58 [doi] PST - ppublish SO - Anesth Analg. 2007 Mar;104(3):638-45. doi: 10.1213/01.ane.0000255046.06058.58.