Artikel
Acute exposure to alcohol suppresses dose-dependently the inflammatory response of human liver cells after induced inflammation
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Veröffentlicht: | 23. Oktober 2017 |
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Gliederung
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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.