ArticleAlcoholism, clinical and experimental research2015
Chronic Alcohol Exposure Enhances Lipopolysaccharide-Induced Lung Injury in Mice: Potential Role of Systemic Tumor Necrosis Factor-Alpha.
Article in Alcoholism, clinical and experimental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- α4 Nicotinic Acetylcholine Receptors in Lipopolysaccharide-Related Lung Inflammation.International journal of molecular sciences · 2024Article
- Article
- Biosensing Platform for the Detection of Biomarkers for ALI/ARDS in Bronchoalveolar Lavage Fluid of LPS Mice Model.Biosensors · 2023Article
- Alcoholic liver disease: a new insight into the pathogenesis of liver disease.Archives of pharmacal research · 2022Review
- Chronic and Binge Alcohol Ingestion Increases Truncated Oxidized Phosphatidylcholines in Mice Lungs Due to Increased Oxidative Stress.Frontiers in physiology · 2022Article
- Extrahepatic factors in hepatic immune regulation.Frontiers in immunology · 2022Review
- Efficacy of human immunoglobulin injection and effects on serum inflammatory cytokines in neonates with acute lung injury.Experimental and therapeutic medicine · 2021Article
- Liver-lung interactions in acute respiratory distress syndrome.Intensive care medicine experimental · 2020Article
- Liver-lung axes in alcohol-related liver disease.Clinical and molecular hepatology · 2020Review
- Innate Immunity and Alcohol.Journal of clinical medicine · 2019Review
- Chronic + binge alcohol exposure promotes inflammation and alters airway mechanics in the lung.Alcohol (Fayetteville, N.Y.) · 2019Article
- Computational/experimental evaluation of liver metastasis post hepatic injury: interactions with macrophages and transitional ECM.Scientific reports · 2019Article
- Neuroinvasion and cognitive impairment in comorbid alcohol dependence and chronic viral infection: An initial investigation.Journal of neuroimmunology · 2019Article
- Organ crosstalk: the potent roles of inflammation and fibrotic changes in the course of organ interactions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Review
- Chronic heavy drinking drives distinct transcriptional and epigenetic changes in splenic macrophages.EBioMedicine · 2019Article
- Plasminogen Activator Inhibitor-1 Is Critical in Alcohol-Enhanced Acute Lung Injury in Mice.American journal of respiratory cell and molecular biology · 2017Article
- Organ-Organ Crosstalk and Alcoholic Liver Disease.Biomolecules · 2017Review
- Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury.World journal of gastroenterology · 2017Review
- The hepatic "matrisome" responds dynamically to injury: Characterization of transitional changes to the extracellular matrix in mice.Hepatology (Baltimore, Md.) · 2017Article
- Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIt is well known that liver and lung injury can occur simultaneously during severe inflammation (e.g., multiple organ failure). However, whether these are parallel or interdependent (i.e., liver-lung axis) mechanisms is unclear. Previous studies have shown that chronic ethanol (EtOH) consumption greatly increases mortality in the setting of sepsis-induced acute lung injury (ALI). The potential contribution of subclinical liver disease in driving this effect of EtOH on the lung remains unknown. Therefore, the purpose of this study was to characterize the impact of chronic EtOH exposure on concomitant liver and lung injury.
methodsMale mice were exposed to EtOH-containing Lieber-DeCarli diet or pair-fed control diet for 6 weeks. Some animals were administered lipopolysaccharide (LPS) 4 or 24 hours prior to sacrifice to mimic sepsis-induced ALI. Some animals received the tumor necrosis factor-alpha (TNF-α)-blocking drug, etanercept, for the duration of alcohol exposure. The expression of cytokine mRNA in lung and liver tissue was determined by quantitative PCR. Cytokine levels in the bronchoalveolar lavage fluid and plasma were determined by Luminex assay.
resultsAs expected, the combination of EtOH and LPS caused liver injury, as indicated by significantly increased levels of the transaminases alanine aminotransferase/aspartate aminotransferase in the plasma and by changes in liver histology. In the lung, EtOH preexposure enhanced pulmonary inflammation and alveolar hemorrhage caused by LPS. These changes corresponded with unique alterations in the expression of pro-inflammatory cytokines in the liver (i.e., TNF-α) and lung (i.e., macrophage inflammatory protein-2 [MIP-2], keratinocyte chemoattractant [KC]). Systemic depletion of TNF-α (etanercept) blunted injury and the increase in MIP-2 and KC caused by the combination of EtOH and LPS in the lung.
conclusionsChronic EtOH preexposure enhanced both liver and lung injury caused by LPS. Enhanced organ injury corresponded with unique changes in the pro-inflammatory cytokine expression profiles in the liver and the lung.
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