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and Interleukin-6 in Monocytes
*Department of Anesthesiology, University Hospital, Rheinisch-Westfälische Technische Hochschule Aachen; and
Department of Cardiology, University Hospital, Mannheim, Germany
Address correspondence and reprint requests to Lothar W. de Rossi, MD, Department of Anesthesiology, University Hospital, Aachen Pauwelsstr, 30, D-52074 Aachen, Germany. Address e-mail to Lderossi{at}ukaachen.de
Anesthetics are known to interfere with the production of inflammatory cytokines. In this study, we investigated the effect of xenon and isoflurane on the lipopolysaccharide (LPS)-induced activation of the nuclear transcription factor (NF)-
B and production of tumor necrosis factor (TNF)-
and interleukin (IL)-6 in vitro. Whole blood was incubated with LPS in the absence or presence of the either xenon (30 and 60 Vol%) and isoflurane (1 and 2 minimum alveolar anesthetic concentration [MAC]). After 4 h, TNF- and IL-6 were assayed in the supernatant. Involvement of NF-B was investigated using isolated monocytes from the blood samples. Whole-cell lysates were prepared, and binding of the NF-B p50 and p65 subunit to its target DNA were measured with an enzyme-linked immunosorbent assay-based NF-B kit. LPS-induced production of TNF- and IL-6 as well as activation of NF-B were significantly increased in the presence of xenon compared with controls. In contrast, isoflurane inhibited the activation of NF-B, which was associated with a decreased production of TNF- and IL-6. Our results demonstrate that xenon and isoflurane have opposite effects on the LPS-induced production of TNF- and IL-6. Furthermore, xenon increases, whereas isoflurane inhibits the activation of NF-B, providing a possible molecular mechanism for the different effects on monocyte TNF- and IL-6 production.
IMPLICATIONS: This study has shown that monocytes respond to lipopolysaccharide (LPS) in the presence of xenon with an increased activation of nuclear transcription factor (NF)-B, whereas isoflurane inhibits LPS-induced activation of NF-B. These findings suggest a possible molecular mechanism for the different effects of both anesthetics on monocyte tumor necrosis factor- and interleukin-6 production.
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