ArticleCritical care medicine2016
Kupffer Cell p38 Mitogen-Activated Protein Kinase Signaling Drives Postburn Hepatic Damage and Pulmonary Inflammation When Alcohol Intoxication Precedes Burn Injury.
Article in Critical care medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Intoxication, inflammaging, and injury: my journey through leukocyte biology.Journal of leukocyte biology · 2026Article
- Post-burn Lung Inflammation Is Associated With Induction of Pulmonary Cathelicidin-related Antimicrobial Peptide and S100a8 in Mice.Journal of burn care & research : official publication of the American Burn Association · 2025Article
- Reducing the excessive inflammation after burn injury in aged mice by maintaining a healthier intestinal microbiome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Reduced Expression of miR-146a Potentiates Intestinal Inflammation following Alcohol and Burn Injury.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Ethanol exacerbates pulmonary complications after burn injury in mice, regardless of frequency of ethanol exposures.Burns : journal of the International Society for Burn Injuries · 2023Article
- Mesenchymal stem cell treatment attenuates liver and lung inflammation after ethanol intoxication and burn injury.Alcohol (Fayetteville, N.Y.) · 2019Article
- Role of HIF-1α in Alcohol-Mediated Multiple Organ Dysfunction.Biomolecules · 2018Review
- Photobiomodulation Therapy Improves Acute Inflammatory Response in Mice: the Role of Cannabinoid Receptors/ATP-Sensitive KMolecular neurobiology · 2018Article
- Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study.Croatian medical journal · 2018Article
- Alcohol and lung injury and immunity.Alcohol (Fayetteville, N.Y.) · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesClinical and animal studies demonstrate that alcohol intoxication at the time of injury worsens postburn outcome. The purpose of this study was to determine the role and mechanism of Kupffer cell derangement in exacerbating postburn end organ damage in alcohol-exposed mice.
designInterventional study.
settingResearch Institute. SUBJECTS: Male C57BL/6 mice.
interventionsAlcohol administered 30 minutes before a 15% scald burn injury. Antecedent Kupffer cell depletion with clodronate liposomes (0.5 mg/kg). p38 mitogen-activated protein kinase inhibition via SB203580 (10 mg/kg). MEASUREMENTS AND MAIN
resultsKupffer cells were isolated 24 hours after injury and analyzed for p38 activity and interleukin-6 production. Intoxicated burned mice demonstrated a two-fold (p < 0.05) elevation of Kupffer cell p38 activation relative to either insult alone, and this corresponded to a 43% (p < 0.05) increase in interleukin-6 production. Depletion of Kupffer cells attenuated hepatic damage as seen by decreases of 53% (p < 0.05) in serum alanine aminotransferase and 74% (p < 0.05) in hepatic triglycerides, as well as a 77% reduction (p < 0.05) in serum interleukin-6 levels compared to matched controls. This mitigation of hepatic damage was associated with a 54% decrease (p < 0.05) in pulmonary neutrophil infiltration and reduced alveolar wall thickening by 45% (p < 0.05). In vivo p38 inhibition conferred nearly identical hepatic and pulmonary protection after the combined injury as mice depleted of Kupffer cells.
conclusionsIntoxication exacerbates postburn hepatic damage through p38-dependent interleukin-6 production in Kupffer cells.
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Registered trials
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