2020
DOI: 10.3390/ijms21218181
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Ethanol Intoxication Alleviates the Inflammatory Response of Remote Organs to Experimental Traumatic Brain Injury

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 withou… Show more

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Cited by 10 publications
(17 citation statements)
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“…The percentage of patients being intoxicated at the time of admission ranges between 30% and 60% in different studies [16]. According to Xu et al [47], alcohol may alleviate the TBI-induced pro-inflammatory response. In our study, 37% of all the patients with TICH were under the influence of alcohol, but their values of NLR and SII did not differ when compared to other patients.…”
Section: Discussionmentioning
confidence: 99%
“…The percentage of patients being intoxicated at the time of admission ranges between 30% and 60% in different studies [16]. According to Xu et al [47], alcohol may alleviate the TBI-induced pro-inflammatory response. In our study, 37% of all the patients with TICH were under the influence of alcohol, but their values of NLR and SII did not differ when compared to other patients.…”
Section: Discussionmentioning
confidence: 99%
“…Importantly, EI also rapidly (already at 3h) dampens the systemic inflammatory response triggered by TBI. In particular, in murineTBI, levels of HMGB1 and IL-6 are decreased in the liver of mice subject to EI/TBI compared to TBI alone (but IL-1β is actually upregulated; [10]) In contrast, in the lungs EI decreases the levels of HMGB1, IL-6, IL-1β and TNF-α, while moderately increasing IL-10 [10]. In line with this evidence, EI is associated with reduced systemic IL-6 levels and less pronounced leukocytosis in human TBI patients [109] and in patients after major traumas (including TBI; [110]), as well as increased levels of IL-10 [111].…”
Section: Discussionmentioning
confidence: 99%
“…In particular, HMGB1, an alarmin located in the nucleus of neurons and glial cells and released upon brain tissue disruption [92, 93], is highly and rapidly elevated in serum after TBI [94, 95]. HMGB1 has been found to contribute not only to local neuroinflammation upon neurotrauma [96, 97] but it is also induced in non-cerebral tissues post TBI and contributes to the subsequent systemic inflammation following TBI [10]. Notably, HMGB1 is also a major inducer of DC maturation, an effect that appears to be relevant in the context of lung injury (through mTOR signaling; [98]) and in liver injury [99].…”
Section: Discussionmentioning
confidence: 99%
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“…Furthermore, the better definition of the inflicted injury on well-defined anatomical regions helps to standardize the injury pattern and thus provides a better if not superior comparison with specific human situations [ 164 ]. Another development towards translational validity is the increasing consideration of various co-morbidities and their adequate modelling such as diabetes, osteoporosis, smoking, alcohol, atherosclerosis or chronic obstructive pulmonary disease in the context of trauma [ 165 167 ].…”
Section: Introductionmentioning
confidence: 99%