ArticleJournal of burn care & research : official publication of the American Burn Association
Propranolol restores the tumor necrosis factor-alpha response of circulating inflammatory monocytes and granulocytes after burn injury and sepsis.
Article in Journal of burn care & research : official publication of the American Burn Association. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
- Murine scald models characterize the role of neutrophils and neutrophil extracellular traps in severe burns.Frontiers in immunology · 2023Article
- Septic predictor index: A novel platform to identify thermally injured patients susceptible to sepsis.Surgery · 2018Article
- Discrete β-adrenergic mechanisms regulate early and late erythropoiesis in erythropoietin-resistant anemia.Surgery · 2017Article
- Perturbed MafB/GATA1 axis after burn trauma bares the potential mechanism for immune suppression and anemia of critical illness.Journal of leukocyte biology · 2016Article
- Effect of beta-blocker therapy on the risk of infections and death after acute stroke--a historical cohort study.PloS one · 2015Article
- Animal models in burn research.Cellular and molecular life sciences : CMLS · 2014Review
- Monocyte subsets and their differentiation tendency after burn injury.Frontiers of medicine · 2013Review
- Retinol binding protein: marker for insulin resistance and inflammation postburn?JPEN. Journal of parenteral and enteral nutrition · 2011Article
- Burn injury dampens erythroid cell production through reprioritizing bone marrow hematopoietic response.The Journal of trauma · 2011Article
- Morphological Changes in Subcutaneous White Adipose Tissue After Severe Burn Injury.Journal of burn care & research : official publication of the American Burn AssociationArticle
- The effect of propranolol on LPS-induced activation of human neutrophils.Doklady. Biochemistry and biophysicsArticle
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6 authors at 1 institution in 1 country.
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Abstract
Beta-adrenergic blockade ameliorates the hypermetabolism and catabolism in severe burn injury. Despite the salutary effects of beta-adrenergic blockade, the immunologic responses that accompany beta-blockade are not known. We have shown that burn sepsis is associated with increased sympathetic activation leading to altered monocytopoiesis and cytokine release in macrophages (MØ). Recent evidence suggests that murine MØ expressing F4/80+Gr1+ are the inflammatory phenotype. Here, we report that propranolol given after burn sepsis modulates the number and function of myeloid cells in circulation. B6D2F1 male mice were divided into sham (S), burn (B), and burn sepsis (BS) groups. Dorsal hair was shaved from S, B, and BS; B and BS received 15% scald burn; BS was inoculated with Pseudomonas Aeruginosa (PA 14, 4000-5000 colony-forming units) at the burn site. Mice from each group were then subjected to two different treatment regimens. One set received subcutaneous injections of propranolol (5 mg/kg body weight) at 24 and 48 hours after the injury while the control groups received saline. Blood was collected by cardiac puncture at 72 hours. The distribution of total F4/80+ monocyte population was determined by flow cytometry. Inflammatory monocyte subset was gated on Gr1+ expression in the F4/80+ fraction. Lipopolysaccharide-stimulated intracellular tumor necrosis factor (TNF)-alpha (ic-TNF) was also measured as an indicator of inflammatory response. The total F4/80+ monocyte fraction was significantly increased in BS (45 +/- 0.8%) vs S and B (10 +/- 0.8%; 9.5 +/- 0.6%). Propranolol treatment for 2 days reduced the number of circulating monocytes by 60% in BS. The mean fluorescent intensity (MFI) of ic-TNF produced per cell (F4/80+Gr1+ MØ) was significantly decreased in B and BS (S: 3043 +/- 213, B: 1638 +/- 343, BS: 1463 +/- 67). Of importance, propranolol treatment partially restored the MFI of ic-TNF (2177 +/- 114) and increased the percentage of inflammatory monocyte subset (F4/80+Gr1+) in BS by 70% compared with saline treatment. In contrast, beta-blockade after BS increased the percentage of granulocytes in circulation (28.4 +/- 3.6% in BS propranolol vs 15.4 +/- 0.3% in BS saline; P < .05) and augmented their TNF production (MFI = 903 +/- 102 in BS propranolol vs 644 +/- 5 in BS saline; P < .05). Propranolol reverses burn sepsis-induced monocytosis and simultaneously increases the number of granulocytes and enhances the inflammatory potential of the granulocytes and inflammatory monocyte subsets in circulation suggesting that monitoring MØ subsets and granulocytes in blood is a reliable biomarker to predict the efficacy of beta-blockade.
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