Journal
ALCOHOL
Volume 47, Issue 3, Pages 223-229Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.alcohol.2013.01.004
Keywords
Lung; Neutrophils; Cytokines; Alcohol; Trauma; Burn
Categories
Funding
- Illinois Excellence in Academic Medicine Grant [R01AA012034, T32AA013527, F32AA018068, F31 AA019913]
- Margaret A. Baima Endowment Fund for Alcohol Research
- Dr. Ralph and Marian C. Falk Medical Research Trust
- Loyola University Chicago Stritch School of Medicine M.D./Ph.D. Program
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Alcohol consumption leads to an exaggerated inflammatory response after burn injury. Elevated levels of interleukin-6 (IL-6) in patients are associated with increased morbidity and mortality after injury, and high systemic and pulmonary levels of IL-6 have been observed after the combined insult of ethanol exposure and burn injury. To further investigate the role of IL-6 in the pulmonary inflammatory response, we examined leukocyte infiltration and cytokine and chemokine production in the lungs of wild-type and IL-6 knockout mice given vehicle or ethanol (1.11 g/kg) and subjected to a sham or 15% total body surface area burn injury. Levels of neutrophil infiltration and neutrophil chemoattractants were increased to a similar extent in wild-type and IL-6 knockout mice 24 h after burn injury. When ethanol exposure preceded the burn injury, however, a further increase of these inflammatory markers was seen only in the wild-type mice. Additionally, signal transducer and activator of transcription-3 (STAT3) phosphorylation did not increase in response to ethanol exposure in the IL-6 knockout mice, in contrast to their wild-type counterparts. Visual and imaging analysis of alveolar wall thickness supported these findings and similar results were obtained by blocking IL-6 with antibody. Taken together, our data suggest a causal relationship between IL-6 and the excessive pulmonary inflammation observed after the combined insult of ethanol and burn injury. (c) 2013 Elsevier Inc. All rights reserved.
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