Tissue lipopolysaccharide-binding protein expression in rats after thermal injury: potential role of TNF-α

Fang, Catherine W. H.; Yao, Yong‐Ming; Zhai, Hao‐Ran; Yu, Yan; Wu, Ye; Lu, Lian-Rong; Zhang, Sheng; Sheng, C Y

doi:10.1016/j.burns.2003.10.007

Cited by 13 publications

(3 citation statements)

References 25 publications

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“…The high expression of LPS-binding protein occurred as a consequence of the elevated circulating LPS-binding protein levels in blood [17]. The complex of LPS bound to LPS-binding protein enables the activation of Kupffer cells via the CD14 receptor [18].…”

Section: Discussionmentioning

confidence: 99%

Hepatic Gene Expression During Endotoxemia

Croner¹,

Hohenberger²,

Jeschke³

2009

Journal of Surgical Research

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Section: Discussionmentioning

confidence: 99%

Hepatic Gene Expression During Endotoxemia

Croner¹,

Hohenberger²,

Jeschke³

2009

Journal of Surgical Research

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“…This was further supported by a report studying early enteral feeding after a scald burn in rats, which significantly improved creatinine clearance, and reduced blood concentrations of TNF [88], despite no changes in circulating endotoxin. In addition, another study revealed that their 35% burn injury produced some perturbations in renal function, as evidenced by significantly increased BUN [89]. However, treatment of burn injury with a monoclonal antibody neutralizing TNF had no effect on BUN but did reduce markers of liver or muscle injury.…”

Section: Immunologic Alterations In Akimentioning

confidence: 99%

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

Burmeister

Gómez

Dubick

2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Trauma-induced acute kidney injury (AKI), such as after hemorrhagic shock (HS) or burn, remains a significant problem in the intensive care unit and is associated with increased mortality. The pathophysiology that drives AKI post-trauma is multi-factorial, and includes both inflammatory and metabolic alterations. Identifying the systemic profile that contributes to AKI is crucial not only for early diagnosis, but also for identifying treatments that improve kidney function and maintaining long-term patient health. In an effort to elucidate this molecular pathophysiology researchers have utilized a variety of animal models including chemically-induced (i.e., cisplatin), blocking renal perfusion (i.e., arterial clamping) and inducing burn or HS. As the latter burn and HS models are unequivocally applicable to studying AKI in the context of traumatic injury, this review will summarize the inflammatory and metabolic insights associated with AKI gained with these animal models. Moreover, novel therapeutic strategies brought forth with these models will be discussed.

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“…Lipopolysaccharide-binding protein (LBP) is a 60kDa acute-phase glycoprotein that is expressed by various tissue cell types following burn injury (1, 2). In stress states such as burn injury and infection, LBP interacts with membrane-bound or soluble CD14, LPS, and toll-like receptor 4 to initiate cellular production of proinflammatory cytokines, immune cell recruitment, and endotoxin clearance.…”

Section: Introductionmentioning

confidence: 99%

Burn-induced Heart Failure: Lipopolysaccharide Binding Protein Improves Burn and Endotoxin-Induced Cardiac Contractility Deficits

Niederbichler

Hoesel

Ipaktchi

et al. 2011

Journal of Surgical Research

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Objective-Burn injury is frequently complicated by bacterial infection. Following burn injury, exposure to endotoxin produces a measurable decrease in cardiomyocyte sarcomere contractile function. Lipopolysaccharide-binding protein (LBP) is an acute phase protein that potentiates the recognition of lipopolysaccharide (LPS) by binding to the lipid A moiety of LPS. In this study we sought to determine the effect of recombinant rat LBP (rLBP) on cardiomyocyte sarcomere function after burn or sham injury in the presence or absence of bacterial endotoxin.Methods-Rats underwent a full-thickness 30% total body surface area scald or sham burn. At 24 hours post injury, cardiomyocytes were isolated, plated at 50,000 cells/well and incubated with 50 μg/mL LPS and rLBP) or chloramphenicol acetyltransferase (BVCat, an irrelevant control protein produced using the same expression system as rLBP) at concentrations by volume of 1, 5, 10, and 30%. Subsets of cardiomyocytes were incubated with 5 % rat serum or 30% rLBP and blocking experiments were conducted using an LBP-like synthetic peptide (LBPK95A). In-vitro sarcomere function was measured using a variable rate video camera system with length detection software.Results-Co-culture of burn and sham injury derived cardiomyocytes with high-dose rLBP in the presence of LPS resulted in a significant reduction to the functional impairment observed in peak sarcomere shortening following exposure to LPS alone. LBP-like peptide LBPK95A at a concentration of 20 μg/mL, in the presence of LPS, abolished the ability of 30 % rLBP and 5% rat serum to restore peak sarcomere shortening of cardiomyocytes isolated following burn injury to levels of function exhibited in the absence of endotoxin exposure. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access

show abstract

Tissue lipopolysaccharide-binding protein expression in rats after thermal injury: potential role of TNF-α

Cited by 13 publications

References 25 publications

Hepatic Gene Expression During Endotoxemia

Hepatic Gene Expression During Endotoxemia

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

Burn-induced Heart Failure: Lipopolysaccharide Binding Protein Improves Burn and Endotoxin-Induced Cardiac Contractility Deficits

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