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German Congress of Orthopedic and Trauma Surgery (DKOU 2017)

24.10. - 27.10.2017, Berlin

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Acute exposure to alcohol suppresses dose-dependently the inflammatory response of human liver cells after induced inflammation

Meeting Abstract

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  • presenting/speaker Katharina Mörs - Department of Trauma, Hand and Reconstructive Surgery, Goethe-University, Frankfurt am Main, Germany
  • Shinwan Kany - Department of Trauma, Hand and Reconstructive Surgery, Goethe-University, Frankfurt am Main, Germany
  • Jason Hörauf - Department of Trauma, Hand and Reconstructive Surgery, Goethe-University, Frankfurt am Main, Germany
  • Nils Wagner - Department of Trauma, Hand and Reconstructive Surgery, Goethe-University, Frankfurt am Main, Germany
  • Mario Perl - Department of Trauma Surgery, Trauma Center Murnau, Murnau, Germany
  • Ingo Marzi - Department of Trauma, Hand and Reconstructive Surgery, Goethe-University, Frankfurt am Main, Germany
  • Borna Relja - Department of Trauma, Hand and Reconstructive Surgery, Goethe-University, Frankfurt am Main, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017). Berlin, 24.-27.10.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocWI22-620

doi: 10.3205/17dkou212, urn:nbn:de:0183-17dkou2122

Published: October 23, 2017

© 2017 Mörs et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

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Objectives: In patients suffering from severe trauma, chronic alcohol misuse has been shown to correlate with poor clinical outcomes, e. g. higher rates of infectious complications. On the other hand, acute alcohol misuse delivered contradicting data, showing none of the negative effects or even exerting positive influences on the clinical course after trauma. Since severe trauma is well described to initially result in a state of systemic inflammation, the observed effects have been linked to the anti-inflammatory potential of acute alcohol exposure. With the liver being one of the first and most severely affected tissues in the context of alcohol misuse, we aimed at analysing time- as well as dose-dependent effects of an acute and sub-acute exposure of human liver cells to alcohol in an in-vitro model of acute inflammation.

Methods: Human Chang Liver (CL) cells were stimulated with either IL-1beta or IL-6 in order to induce a state of inflammation, and were subsequently treated with either low or high-dose alcohol (85 mM, LoD or 170 mM, HiD, respectively) for 1h (acute) or 72h (sub-acute). Neutrophil adhesion to CL monolayers, production of reactive oxygen species (ROS) and cell death were analyzed. Additionally, the release of IL-6 and IL-1beta- was determined by ELISA.

Results and Conclusion: Acute LoD alcohol significantly diminished IL-1beta-induced IL-6 (1536.00±63.68 vs. 774.50±222.10 ng/ml, p<0.05) and IL-6-induced IL-1beta-release (6.41±2.35 vs. 1.14±0.54 ng/ml, p<0.05), respectively. HiD alcohol as well as sub-acute alcohol did not influence the cytokine release markedly. Acute LoD alcohol significantly improved cell-survival (78.15% vs. 83.42%, p<0.05) as shown by decreased formation of ROS (78.33 vs. 70.07%, p<0.05). Treatment with HiD acute alcohol or sub-acute setting showed no significant changes. Neutrophil adhesion to stimulated CL cells significantly decreased after acute (111.40% vs. 82.07%, p<0.05) as well as sub-acute (122.90±8.93% vs. 88.64%, p<0.05) exposure to alcohol. This effect was observed independently of the alcohol dose.