Acute ethanol administration results in a protective cytokine and neuroinflammatory profile in traumatic brain injury.

Autor: Chandrasekar A; Dept. of Neurology, University of Ulm, School of Medicine, Germany. Electronic address: akila.chandrasekar@uni-ulm.de., Heuvel FO; Dept. of Neurology, University of Ulm, School of Medicine, Germany., Palmer A; Institute of Clinical and Experimental Trauma Immunology, University Ulm, Ulm, Germany. Electronic address: annette.palmer@uniklinik-ulm.de., Linkus B; Dept. of Neurology, University of Ulm, School of Medicine, Germany. Electronic address: birgit.linkus@uni-ulm.de., Ludolph AC; Dept. of Neurology, University of Ulm, School of Medicine, Germany. Electronic address: albert.ludolph@rku.de., Boeckers TM; Dept. of Anatomy and Cell Biology, Ulm University, School of Medicine, Germany. Electronic address: tobias.boeckers@uni-ulm.de., Relja B; Dept. of General and Visceral Surgery, Goethe University, Frankfurt, Germany. Electronic address: info@bornarelja.com., Huber-Lang M; Institute of Clinical and Experimental Trauma Immunology, University Ulm, Ulm, Germany. Electronic address: markus.huber-lang@uniklinik-ulm.de., Roselli F; Dept. of Neurology, University of Ulm, School of Medicine, Germany. Electronic address: francesco.roselli@uni-ulm.de.
Jazyk: angličtina
Zdroj: International immunopharmacology [Int Immunopharmacol] 2017 Oct; Vol. 51, pp. 66-75. Date of Electronic Publication: 2017 Aug 12.
DOI: 10.1016/j.intimp.2017.08.002
Abstrakt: Ethanol intoxication is a common comorbidity in traumatic brain injury. To date, the effect of ethanol on TBI pathogenic cascades and resulting outcomes remains debated. A closed blunt weight-drop murine TBI model has been implemented to investigate behavioral (by sensorimotor and neurological tests), and neuro-immunological (by tissue cytokine arrays and immuno-histology) effects of ethanol intoxication on TBI. The effect of the occurrence of traumatic intracerebral hemorrhage was also studied. The results indicate that ethanol pretreatment results in a faster and better recovery after TBI with reduced infiltration of leukocytes and reduced microglia activation. These outcomes correspond to reduced parenchymal levels of GM-CSF, IL-6 and IL-3 and to the transient upregulation of IL-13 and VEGF, indicating an early shift in the cytokine profile towards reduced inflammation. A significant difference in the cytokine profile was still observed 24h post injury in the ethanol pretreated mice, as shown by the delayed peak in IL-6 and by the suppression of GM-CSF, IFN-γ, and IL-3. Seven days post-injury, ethanol-pretreated mice displayed a significant decrease both in CD45+ cells infiltration and in microglial activation. On the other hand, in the case of traumatic intracerebral hemorrhage, the cytokine profile was dominated by KC, CCL5, M-CSF and several interleukins and ethanol pretreatment did not produce any modification. We can thus conclude that ethanol intoxication suppresses the acute neuro-inflammatory response to TBI, an effect which is correlated with a faster and complete neurological recovery, whereas, the presence of traumatic intracerebral hemorrhage overrides the effects of ethanol.
(Copyright © 2017 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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