TY  - JOUR
A1  - Maraslioglu, Miriam
A1  - Oppermann, Elsie
A1  - Blattner, Carolin
A1  - Weber, Roxane
A1  - Henrich, Dirk
A1  - Jobin, Christian
A1  - Schleucher, Elke
A1  - Marzi, Ingo
A1  - Lehnert, Mark
T1  - Chronic ethanol feeding modulates inflammatory mediators, activation of nuclear factor-κB, and responsiveness to endotoxin in murine Kupffer cells and circulating leukocytes
T2  - Mediators of inflammation
N2  - Chronic ethanol abuse is known to increase susceptibility to infections after injury, in part, by modification of macrophage function. Several intracellular signalling mechanisms are involved in the initiation of inflammatory responses, including the nuclear factor-κB (NF-κB) pathway. In this study, we investigated the systemic and hepatic effect of chronic ethanol feeding on in vivo activation of NF-κB in NF-κB(EGFP) reporter gene mice. Specifically, the study focused on Kupffer cell proinflammatory cytokines IL-6 and TNF-α and activation of NF-κB after chronic ethanol feeding followed by in vitro stimulation with lipopolysaccharide (LPS). We found that chronic ethanol upregulated NF-κB activation and increased hepatic and systemic proinflammatory cytokine levels. Similarly, LPS-stimulated IL-1 β release from whole blood was significantly enhanced in ethanol-fed mice. However, LPS significantly increased IL-6 and TNF-α levels. These results demonstrate that chronic ethanol feeding can improve the responsiveness of macrophage LPS-stimulated IL-6 and TNF-α production and indicate that this effect may result from ethanol-induced alterations in intracellular signalling through NF-κB. Furthermore, LPS and TNF-α stimulated the gene expression of different inflammatory mediators, in part, in a NF-κB-dependent manner.
Y1  - 2014
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/35289
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-352893
SN  - 1466-1861
SN  - 0962-9351
N1  - Copyright © 2014 Miriam Maraslioglu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
VL  - 2014
IS  - Article ID 808695
SP  - 1
EP  - 16
PB  - Hindawi Publishing Corp.
CY  - Sylvania, Ohio
ER  -