The Significance of Changes in High Mobility Group-1 Protein mRNA Expression in Rats After Thermal Injury
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There has been a widespread impression that tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) mediate the toxicity of high doses of lipopolysaccharide (LPS, endotoxin) and are key factors in septic shock. However, the clinical efficacy of treatment with antagonists of TNF-α and IL-1β is still controversial, suggesting that mediators other than TNF-α and IL-1β might contribute causally to endotoxin-induced death. Recent studies implicated high mobility group-1 (HMG-1) protein as a late mediator of endotoxin lethality in mice. However, the role of HMG-1 in mediating multiple organ damage-associating trauma has not been studied. This study was designed to investigate changes in HMG-1 gene expression in vital organs, and its potential role in mediating multiple organ damage following major burns. Wistar rats were subjected to a 35 percent full-thickness thermal injury, and randomly divided into three groups as follows: normal controls (n = 7), thermal injury (n = 24), and recombinant bactericidal/permeability-increasing protein (rBPI21) treatment (n = 12). Tissue samples from liver and lungs were collected to measure tissue endotoxin levels and HMG-1 mRNA expression. In addition, blood samples were obtained for measurement of organ function parameters. Our data demonstrated a significant increase in HMG-1 gene expression in tissues at 24 h postburn, which remained markedly elevated up to 72 h after thermal injury (P < 0.05–0.01). Treatment with rBPI21 could significantly decrease tissue HMG-1 mRNA expression in the liver and lung (P < 0.01). In addition, there were high positive correlations between hepatic HMG-1 mRNA and serum aminoleucine transferase (ALT) and aspartate aminotransferase (AST) levels, and also between pulmonary HMG-1 mRNA and myeloperoxidase activities (P < 0.05–0.01). Taken together, these findings indicate that thermal injury per se can markedly enhance HMG-1 gene expression in various organs. Up-regulation of HMG-1 expression may be involved in the pathogenesis of endogenous endotoxin-mediated multiple organ damage secondary to major burns.Keywords:
Alpha (finance)
Lipid A
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Septic shock is a common syndrome. In recent years, the incidence of septic shock increases year by year, and the mortality rate of septic shock is high. More and more medical workers and scho- lars begin to pay attention to septic shock's occurrence, development, diagnosis and treatment, expecting the standardized treatment to reduce the mortality. The current review is to update the management of sepsis and septic shock.
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Gram-Negative Bacteria
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The role of skullcapflavone II in pneumonia was investigated using lipopolysaccharide treated human lung fibroblasts WI-38 cells as a model. Lipopolysaccharide treatment led to decreased cell viability, increased cell apoptosis and inflammation. Exposure of these lipopolysaccharide-treated cells to skullcapflavone II resulted in amelioration of cytotoxic effects of the lipopolysaccharide. The reduced IκBα expression and enhanced p-IκBα and p-p65 in WI-38 cells caused by the lipopolysaccharide treatment were reversed by skullcapflavone II. In conclusion, skullcapflavone II exerts antiapoptotic and anti-inflammatory effects on lipopolysaccharide-induced WI-38 through inhibition of NF-κB pathway.
Viability assay
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Cultured rat Kupffer cells were incubated in presence of biologically tritiated Salmonella abortus equi lipopolysaccharide. Uptake of lipopolysaccharide increased rapidly during the first 2 h of incubation and then levelled off. Within the first h of incubation 10(6) Kupffer cells were able to ingest up to 18 micrograms lipopolysaccharide. Kupffer cells metabolised lipopolysaccharide and released lipopolysaccharide-related substances, but neither the cell-associated lipopolysaccharide nor the released lipopolysaccharide products were detoxified, as measured by the mouse lethality test.
Kupffer cell
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The mortality rate of septic shock remains high. The guidelines of the Surviving Sepsis Campaign were published in 2004 and were revised in 2008. Steroid therapy is prominent in the guidelines but remains controversial. In this review, steroid therapy for septic shock is discussed with various landmark papers.
Surviving Sepsis Campaign
Shock therapy
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Castor oil, lipopolysaccharide of Escherichia coli, and endotoxin of Salmonella typhimurium were used for inducing diarrhoea in sham operated or caecectomized mice. Copious diarrhoea was induced by lipopolysaccharide (LPS) in caecectomized mice. Characteristics of diarrhoea induced by castor oil were not different between the two groups. It is concluded that caecectomized mice may be a good model to study lipopolysaccharide-induced diarrhoea.
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Mild alkaline hydrolysis of lipopolysaccharide endotoxin enhances its mitogencity for murine B cells
Mild alkaline hydrolysis was found to enhance the mitogenicity of lipopolysaccharide endotoxin for murine B lymphocytes. Alkaline treated lipopolysaccharide also retained its property as a polyclonal activator. Whereas this treatment reduced the lethality of endotoxin for mice, its toxicity for lymphocytes cultured in the absence of fetal calf serum was increased. Lipid analysis indicated that there were no significant changes in the fatty acids of lipid A, but particle size was significantly reduced and the material was more homogeneous and soluble than untreated lipopolysaccharide. The relationship of these effect on the structure of lipopolysaccharide endotoxin to the mechanism of B-lymphocyte activation is discussed.
Lipid A
Polyclonal antibodies
Alkaline hydrolysis
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Objective To observe the changes of plasma elastin peptide (EP) level in septic shock patients, and to investigate the effects that EP engender on the hemodynamics during septic shock.Methods Blood samples for EP measurement by ELISA were collected from 18 septic shock patients, 36 non-septic patients and 18 healthy persons. Results The plasma EP level during shock persistence period in septic patients was significantly higher than that in non-septic shock and healthy patients, which was similar in the latter two groups. The plasma EP level during shock recovery period was significantly lower than that during shock persistence period in septic patients. Conclusion The plasma EP level during shock persistence period in septic shock patients was significantly elevated, it may be invalved in the hemodynamic changes during septic shock.
Persistence (discontinuity)
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