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Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study

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Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study. / Mörs, Katharina; Kany, Shinwan; Hörauf, Jason-Alexander; Wagner, Nils; Neunaber, Claudia; Perl, Mario; Marzi, Ingo; Relja, Borna.

in: CROAT MED J, Jahrgang 59, Nr. 2, 30.04.2018, S. 46-55.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Mörs, K, Kany, S, Hörauf, J-A, Wagner, N, Neunaber, C, Perl, M, Marzi, I & Relja, B 2018, 'Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study', CROAT MED J, Jg. 59, Nr. 2, S. 46-55. https://doi.org/10.3325/cmj.2018.59.46

APA

Mörs, K., Kany, S., Hörauf, J-A., Wagner, N., Neunaber, C., Perl, M., Marzi, I., & Relja, B. (2018). Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study. CROAT MED J, 59(2), 46-55. https://doi.org/10.3325/cmj.2018.59.46

Vancouver

Mörs K, Kany S, Hörauf J-A, Wagner N, Neunaber C, Perl M et al. Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study. CROAT MED J. 2018 Apr 30;59(2):46-55. https://doi.org/10.3325/cmj.2018.59.46

Bibtex

@article{28edadd98c614c6e9616f3a95ee88139,
title = "Suppression of the interleukin-1{\ss}-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study",
abstract = "AIM: To evaluate protective immunosuppressive dose and time-dependent effects of ethanol in an in vitro model of acute inflammation in human Chang liver cells.METHOD: The study was performed in 2016 and 2017 in the research laboratory of the Department of Trauma, Hand and Reconstructive Surgery, the University Hospital of the Goethe-University Frankfurt. Chang liver cells were stimulated with either interleukin (IL)-1β or IL-6 and subsequently treated with low-dose ethanol (85 mmol/L) or high-dose ethanol (170 mmol/L) for one hour (acute exposure) or 72 hours (subacute exposure). IL-6 and IL-1β release were determined by enzyme-linked immunosorbent assay. Neutrophil adhesion to Chang liver monolayers, production of reactive oxygen species, and apoptosis or necrosis were analyzed.RESULTS: Contrary to high-dose ethanol, acute low-dose ethanol exposure significantly reduced IL-1β-induced IL-6 and IL-6-induced IL-1β release (P<0.05). Subacute ethanol exposure did not change proinflammatory cytokine release. Acute low-dose ethanol exposure significantly decreased inflammation-induced formation of reactive oxygen species (P<0.05) and significantly improved cell survival (P<0.05). Neither acute nor subacute high-dose ethanol exposure significantly changed inflammation-induced changes in reactive oxygen species or survival. Acute and subacute ethanol exposure, independently of the dose, significantly decreased neutrophil adhesion to inflamed Chang liver cells (P<0.05).CONCLUSION: Acute treatment of inflamed Chang liver cells with ethanol showed its immunosuppressive potential. However, the observed effects were limited to low-dose setting, indicating the relevance of ethanol dose in the modulation of inflammatory cell response.",
keywords = "Cell Adhesion/drug effects, Cell Survival/drug effects, Ethanol/pharmacology, Humans, Inflammation/metabolism, Interleukin-1beta/metabolism, Interleukin-6/metabolism, Liver/drug effects, Neutrophils/physiology, Reactive Oxygen Species/metabolism",
author = "Katharina M{\"o}rs and Shinwan Kany and Jason-Alexander H{\"o}rauf and Nils Wagner and Claudia Neunaber and Mario Perl and Ingo Marzi and Borna Relja",
year = "2018",
month = apr,
day = "30",
doi = "10.3325/cmj.2018.59.46",
language = "English",
volume = "59",
pages = "46--55",
number = "2",

}

RIS

TY - JOUR

T1 - Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study

AU - Mörs, Katharina

AU - Kany, Shinwan

AU - Hörauf, Jason-Alexander

AU - Wagner, Nils

AU - Neunaber, Claudia

AU - Perl, Mario

AU - Marzi, Ingo

AU - Relja, Borna

PY - 2018/4/30

Y1 - 2018/4/30

N2 - AIM: To evaluate protective immunosuppressive dose and time-dependent effects of ethanol in an in vitro model of acute inflammation in human Chang liver cells.METHOD: The study was performed in 2016 and 2017 in the research laboratory of the Department of Trauma, Hand and Reconstructive Surgery, the University Hospital of the Goethe-University Frankfurt. Chang liver cells were stimulated with either interleukin (IL)-1β or IL-6 and subsequently treated with low-dose ethanol (85 mmol/L) or high-dose ethanol (170 mmol/L) for one hour (acute exposure) or 72 hours (subacute exposure). IL-6 and IL-1β release were determined by enzyme-linked immunosorbent assay. Neutrophil adhesion to Chang liver monolayers, production of reactive oxygen species, and apoptosis or necrosis were analyzed.RESULTS: Contrary to high-dose ethanol, acute low-dose ethanol exposure significantly reduced IL-1β-induced IL-6 and IL-6-induced IL-1β release (P<0.05). Subacute ethanol exposure did not change proinflammatory cytokine release. Acute low-dose ethanol exposure significantly decreased inflammation-induced formation of reactive oxygen species (P<0.05) and significantly improved cell survival (P<0.05). Neither acute nor subacute high-dose ethanol exposure significantly changed inflammation-induced changes in reactive oxygen species or survival. Acute and subacute ethanol exposure, independently of the dose, significantly decreased neutrophil adhesion to inflamed Chang liver cells (P<0.05).CONCLUSION: Acute treatment of inflamed Chang liver cells with ethanol showed its immunosuppressive potential. However, the observed effects were limited to low-dose setting, indicating the relevance of ethanol dose in the modulation of inflammatory cell response.

AB - AIM: To evaluate protective immunosuppressive dose and time-dependent effects of ethanol in an in vitro model of acute inflammation in human Chang liver cells.METHOD: The study was performed in 2016 and 2017 in the research laboratory of the Department of Trauma, Hand and Reconstructive Surgery, the University Hospital of the Goethe-University Frankfurt. Chang liver cells were stimulated with either interleukin (IL)-1β or IL-6 and subsequently treated with low-dose ethanol (85 mmol/L) or high-dose ethanol (170 mmol/L) for one hour (acute exposure) or 72 hours (subacute exposure). IL-6 and IL-1β release were determined by enzyme-linked immunosorbent assay. Neutrophil adhesion to Chang liver monolayers, production of reactive oxygen species, and apoptosis or necrosis were analyzed.RESULTS: Contrary to high-dose ethanol, acute low-dose ethanol exposure significantly reduced IL-1β-induced IL-6 and IL-6-induced IL-1β release (P<0.05). Subacute ethanol exposure did not change proinflammatory cytokine release. Acute low-dose ethanol exposure significantly decreased inflammation-induced formation of reactive oxygen species (P<0.05) and significantly improved cell survival (P<0.05). Neither acute nor subacute high-dose ethanol exposure significantly changed inflammation-induced changes in reactive oxygen species or survival. Acute and subacute ethanol exposure, independently of the dose, significantly decreased neutrophil adhesion to inflamed Chang liver cells (P<0.05).CONCLUSION: Acute treatment of inflamed Chang liver cells with ethanol showed its immunosuppressive potential. However, the observed effects were limited to low-dose setting, indicating the relevance of ethanol dose in the modulation of inflammatory cell response.

KW - Cell Adhesion/drug effects

KW - Cell Survival/drug effects

KW - Ethanol/pharmacology

KW - Humans

KW - Inflammation/metabolism

KW - Interleukin-1beta/metabolism

KW - Interleukin-6/metabolism

KW - Liver/drug effects

KW - Neutrophils/physiology

KW - Reactive Oxygen Species/metabolism

U2 - 10.3325/cmj.2018.59.46

DO - 10.3325/cmj.2018.59.46

M3 - SCORING: Journal article

C2 - 29740988

VL - 59

SP - 46

EP - 55

IS - 2

ER -