ArticleAlcohol (Fayetteville, N.Y.)2007
Acute alcohol intake impairs lung inflammation by changing pro- and anti-inflammatory mediator balance.
Article in Alcohol (Fayetteville, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- Acute Intoxication With Alcohol Reduces Trauma-Induced Proinflammatory Response and Barrier Breakdown in the LungFrontiers in immunology · 2022Article
- Ethanol Intoxication Alleviates the Inflammatory Response of Remote Organs to Experimental Traumatic Brain Injury.International journal of molecular sciences · 2020Article
- Article
- Alcohol-dependent pulmonary inflammation: A role for HMGB-1.Alcohol (Fayetteville, N.Y.) · 2019Article
- Alcohol and cannabis use alter pulmonary innate immunity.Alcohol (Fayetteville, N.Y.) · 2019Article
- Effects of binge alcohol consumption on sleep and inflammation in healthy volunteers.The Journal of international medical research · 2018Observational
- Beneficial effects of low alcohol exposure, but adverse effects of high alcohol intake on glymphatic function.Scientific reports · 2018Article
- Neuroimmune Interface in the Comorbidity between Alcohol Use Disorder and Major Depression.Frontiers in immunology · 2016Review
- Globular adiponectin inhibits ethanol-induced reactive oxygen species production through modulation of NADPH oxidase in macrophages: involvement of liver kinase B1/AMP-activated protein kinase pathway.Molecular pharmacology · 2014Article
- Increased plasma corticosterone contributes to the development of alcoholic fatty liver in mice.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Effects of prenatal ethanol exposure on the lungs of postnatal lambs.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Laboratory models available to study alcohol-induced organ damage and immune variations: choosing the appropriate model.Alcoholism, clinical and experimental research · 2010Review
- Ethanol exposure impairs LPS-induced pulmonary LIX expression: alveolar epithelial cell dysfunction as a consequence of acute intoxication.Alcoholism, clinical and experimental research · 2009Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have shown that alcohol (ethanol [EtOH]) intoxication impairs lung immunity by affecting cytokines pivotal to the inflammatory process. The objective of this study was to test the hypothesis that acute alcohol intoxication impairs lung innate immunity by downregulating the expression of proinflammatory mediators while simultaneously upregulating anti-inflammatory mediators. EtOH was administered to the mice 0.5h prior to an intratracheal injection of Escherichia coli lipopolysaccharide (LPS). The animals were killed either 4 or 24h after LPS to recover plasma, lungs, and bronchoalveolar lavage fluid. Lung inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, macrophage inhibitory factor (MIF), IL-10, TGF-beta, and receptors for TNF-alpha, IL-1beta, IL-6, and TGF-beta as well as glycoprotein (gp)130 and corticosterone (CS) levels were evaluated at mRNA and protein level. While the mRNA expression and the soluble TNF-Rp55 levels were significantly upregulated by EtOH, LPS-induced TNF-alpha activity, TNF-Rp55 mRNA expression, and soluble TNF-Rp55 levels were significantly suppressed. The LPS-induced expression of IL-1beta, IL-6, MIF, gp130, and receptors IL-1RI, IL-1RII, and IL-6Ralpha were also significantly impaired by EtOH. EtOH increased significantly the basal IL-10 activity at 3h, which continued to remain elevated even at 24h. The EtOH effect on IL-10 activity persisted even in LPS-challenged mice. EtOH and LPS augmented lung CS levels independently of each other. EtOH suppressed upregulation of TGF-beta1 mRNA expression by LPS and blocked completely LPS-induced TGF-beta1 secretion. In conclusion, the data suggest that the suppression of acute lung inflammation by EtOH intoxication is largely due to impairment by EtOH of proinflammatory cytokine signaling at the levels of cytokine expression and secretion as well as receptor expression and soluble receptor activity. The augmentation by EtOH of anti-inflammatory mediators' secretion most likely shifts the cytokine balance in the anti-inflammatory direction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.