Please use this identifier to cite or link to this item:
http://dx.doi.org/10.25673/36367
Title: | Ethanol intoxication alleviates the inflammatory response of remote organs to experimental traumatic brain injury |
Author(s): | Xu, Baolin Chandrasekar, Akila Heuvel, Florian Olde Powerski, Maciej Janusz Nowak, Aleksander Noack, Laurens Omari, Jazan Huber-Lang, Markus Roselli, Francesco Relja, Borna |
Issue Date: | 2020 |
Type: | Article |
Language: | English |
URN: | urn:nbn:de:gbv:ma9:1-1981185920-365990 |
Subjects: | Inflammation TBI Alcohol Cytokines |
Abstract: | Traumatic brain injury (TBI) may cause damage to distant organs. Acute ethanol intoxication (EI) induces complex local and systemic anti-inflammatory effects and influences the early outcomes of traumatized patients. Here, we evaluated its effects on the BI-induced expression of local inflammatory mediators in the trauma-remote organs the lungs and liver. Male mice were exposed to ethanol as a single oral dose (5g·kg–1, 32%) before inducing a moderate blunt TBI. Sham groups underwent the same procedures without TBI. Ether 3 or 6h after the TBI, the lung and liver were collected. The gene expression of HMGB1, IL-6, MMP9, IL-1β, and TNF as well as the homogenate protein levels of receptor for advanced glycation end products (RAGE), IL-6, IL-1β, and IL-10 were analyzed. Liver samples were immunohistologically stained for HMGB1. EI decreased the gene expressions of the proinflammatory markers HMGB1, IL-6, and MMP9 in the liver upon TBI. In line with the reduced gene expression, the TBI-induced protein expression of IL-6 in liver tissue homogenates was significantly reduced by EI at 3h after TBI. While the histological HMGB1 expression was enhanced by TBI, the RAGE protein expression in the liver tissue homogenates was diminished after TBI. EI reduced the histological HMGB1 expression and enhanced the hepatic RAGE protein expression at 6h post TBI. With regard to the lungs, EI significantly reduced the gene expressions of HMGB1, IL-6, IL-1β, and TNF upon TBI, without significantly affecting the protein expression levels of inflammatory markers (RAGE, IL-6, IL-1β, and IL-10). At the early stage of TBI-induced inflammation, the gene expression of inflammatory mediators in both the lungs and liver is susceptible to ethanol-induced remote effects. Taken together, EI may alleviate the TBI-induced pro-inflammatory response in the trauma-distant organs, the lungs and liver, via the HMGB1-RAGE axis. |
URI: | https://opendata.uni-halle.de//handle/1981185920/36599 http://dx.doi.org/10.25673/36367 |
Open Access: | Open access publication |
License: | (CC BY-SA 4.0) Creative Commons Attribution ShareAlike 4.0 |
Sponsor/Funder: | DFG-Publikationsfonds 2020 |
Journal Title: | International journal of molecular sciences |
Publisher: | Molecular Diversity Preservation International |
Publisher Place: | Basel |
Volume: | 21 |
Issue: | 21 |
Original Publication: | 10.3390/ijms21218181 |
Page Start: | 1 |
Page End: | 14 |
Appears in Collections: | Medizinische Fakultät (OA) |
Files in This Item:
File | Description | Size | Format | |
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Xu et al._Ethanol_2020.pdf | Zweitveröffentlichung | 1.36 MB | Adobe PDF | View/Open |