PMID- 19032551
OWN - NLM
STAT- MEDLINE
DCOM- 20090220
LR  - 20211020
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 155
IP  - 2
DP  - 2009 Feb
TI  - The volatile anaesthetic sevoflurane attenuates lipopolysaccharide-induced injury 
      in alveolar macrophages.
PG  - 224-30
LID - 10.1111/j.1365-2249.2008.03807.x [doi]
AB  - Acute lung injury (ALI) is a well-defined inflammation whereby alveolar 
      macrophages play a crucial role as effector cells. As shown previously in 
      numerous experimental approaches, volatile anaesthetics might reduce the degree 
      of injury in pre- or post-conditioning set-ups. Therefore, we were interested to 
      evaluate the effect of the application of the volatile anaesthetic sevoflurane on 
      alveolar macrophages regarding the expression of inflammatory mediators upon 
      lipopolysaccharide (LPS) stimulation in vitro. Alveolar macrophages were 
      stimulated with LPS. Two hours later, cells were exposed additionally to air 
      (control) or to sevoflurane-containing air for 4, 6, 8, 12 or 24 h. Tumour 
      necrosis factor (TNF)-alpha, cytokine-induced neutrophil chemoattractant-1 
      (CINC-1), macrophage-inflammatory protein-2 (MIP-2) and monocyte chemoattractant 
      protein-1 (MCP-1) proteins were determined and chemotaxis assays were performed. 
      To evaluate possible cellular signalling pathways phosphorylation of the kinases 
      extracellular-regulated kinase (ERK) and Akt was assessed. In the early phase of 
      sevoflurane post-conditioning expression of TNF-alpha, CINC-1, MIP-2 and MCP-1 
      was attenuated, leading to a diminished chemotaxis reaction for neutrophils. 
      Phosphorylation of ERK seems to be a possible cellular mechanism in the 
      sevoflurane-induced protection in vitro. Pharmacological post-conditioning of 
      alveolar macrophages with sevoflurane immunmodulates the inflammatory response 
      upon stimulation with endotoxin. This might be a possible option for a 
      therapeutical approach in ALI.
FAU - Steurer, M
AU  - Steurer M
AD  - Institute of Physiology, Zurich Center of Integrative Human Physiology, Zurich, 
      Switzerland.
FAU - Schlapfer, M
AU  - Schlapfer M
FAU - Steurer, M
AU  - Steurer M
FAU - Z'graggen, B Roth
AU  - Z'graggen BR
FAU - Booy, C
AU  - Booy C
FAU - Reyes, L
AU  - Reyes L
FAU - Spahn, D R
AU  - Spahn DR
FAU - Beck-Schimmer, B
AU  - Beck-Schimmer B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20081120
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Anesthetics, Inhalation)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Cxcl1 protein, rat)
RN  - 0 (Cxcl2 protein, rat)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Methyl Ethers)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 38LVP0K73A (Sevoflurane)
SB  - IM
MH  - Acute Lung Injury/metabolism/pathology
MH  - Anesthetics, Inhalation/*pharmacology
MH  - Animals
MH  - Cell Line
MH  - Chemokine CCL2/biosynthesis
MH  - Chemokine CXCL1/biosynthesis
MH  - Chemokine CXCL2/biosynthesis
MH  - Chemotaxis, Leukocyte/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Lipopolysaccharides/*antagonists & inhibitors/pharmacology
MH  - Macrophage Inflammatory Proteins/*biosynthesis
MH  - Macrophages, Alveolar/*drug effects/metabolism
MH  - Methyl Ethers/*pharmacology
MH  - Rats
MH  - Sevoflurane
MH  - Signal Transduction/drug effects
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC2675253
EDAT- 2008/11/27 09:00
MHDA- 2009/02/21 09:00
PMCR- 2010/02/01
CRDT- 2008/11/27 09:00
PHST- 2008/11/27 09:00 [pubmed]
PHST- 2009/02/21 09:00 [medline]
PHST- 2008/11/27 09:00 [entrez]
PHST- 2010/02/01 00:00 [pmc-release]
AID - CEI3807 [pii]
AID - 10.1111/j.1365-2249.2008.03807.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2009 Feb;155(2):224-30. doi: 10.1111/j.1365-2249.2008.03807.x. 
      Epub 2008 Nov 20.