TY - JOUR A1 - Mörs, Katharina A1 - Kany, Shinwan Salah A1 - Hörauf, Jason-Alexander A1 - Wagner, Nils A1 - Neunaber, Claudia A1 - Perl, Mario A1 - Marzi, Ingo A1 - Relja, Borna 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 T1 - Suzbija li akutna ili subakutna izloženost alkoholu upalni odgovor Chang stanica jetre izazvan interleukinom-1β? : in vitro istraživanje T2 - Croatian medical journal 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 stimu - lated with either interleukin (IL)-1β or IL-6 and subsequent - ly 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 de - termined by enzyme-linked immunosorbent assay. Neu - trophil 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 etha - nol 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 inflammationinduced 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. N2 - Cilj: Odrediti protektivne imunosupresijske učinke etanola ovisne o dozi i vremenu u in vitro modelu akutne upale u ljudskim Chang stanicama jetre. Postupci: Istraživanje je provedeno 2016. i 2017. u istraživačkom laboratoriju Zavoda za traumatologiju, kirurgiju ruke i rekonstruktivnu kirurgiju Bolnice Sveučilišta Goethe u Frankfurtu. Chang stanice jetre stimulirane su ili interleukinom-1β ili interleukinom-6 te tretirane niskom (85 mmol/L) ili visokom dozom etanola (170 mmol/L) jedan sat (akutna izloženost) ili 72 sata (subakutna izloženost). Otpuštanje IL-6 i IL-1β određeno je enzimskim imunotestom. Također smo analizirali adheziju neutrofila na monoslojeve Chang stanica jetre, proizvodnju reaktivnih vrsta kisika i apoptozu ili nekrozu. Rezultati: Nasuprot visokoj dozi, niska doza etanola značajno je smanjila otpuštanje interleukina-6 izazvano interleukinom-1β i otpuštanje interleukina-1β izazvano interleukinom-6 (P < 0,05). Subakutna izloženost etanolu nije promijenila proinflamatorno otpuštanje citokina. Akutna niska doza etanola značajno je smanjila formiranje reaktivnih vrsta kisika izazvano upalom (P < 0.05) i značajno je poboljšala preživljenje stanica (P < 0.05). Ni akutna ni subakutna visoka doza etanola nisu značajno utjecale na promjene izazvane upalom kod reaktivnih vrsta kisika i preživljenja stanica. Akutna i subakutna doza etanola, neovisno o dozi, značajno su smanjile adheziju neutrofila na upaljene Chang stanice jetre (P < 0.05). Zaključak: Akutna izloženost Chang stanica jetre etanolu pokazala je njegov imunosupresivni potencijal. Međutim, takvi učinci zabilježeni su samo za nisku dozu, upućujući na važnost doze etanola u modulaciji upalnog odgovora stanica. Y1 - 2018 UR - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/46693 UR - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-466930 SN - 1332-8166 SN - 0353-9504 N1 - This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. VL - 59 IS - 2 SP - 46 EP - 55 PB - Univ. of Zagreb, School of Medicine CY - Zagreb ER -