scispace - formally typeset
Journal ArticleDOI

HMG-1 as a Late Mediator of Endotoxin Lethality in Mice

Reads0
Chats0
TLDR
High mobility group-1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1, and showed increased serum levels after endotoxin exposure, suggesting that this protein warrants investigation as a therapeutic target.
Abstract
Endotoxin, a constituent of Gram-negative bacteria, stimulates macrophages to release large quantities of tumor necrosis factor (TNF) and interleukin-1 (IL-1), which can precipitate tissue injury and lethal shock (endotoxemia). Antagonists of TNF and IL-1 have shown limited efficacy in clinical trials, possibly because these cytokines are early mediators in pathogenesis. Here a potential late mediator of lethality is identified and characterized in a mouse model. High mobility group-1 (HMG-1) protein was found to be released by cultured macrophages more than 8 hours after stimulation with endotoxin, TNF, or IL-1. Mice showed increased serum levels of HMG-1 from 8 to 32 hours after endotoxin exposure. Delayed administration of antibodies to HMG-1 attenuated endotoxin lethality in mice, and administration of HMG-1 itself was lethal. Septic patients who succumbed to infection had increased serum HMG-1 levels, suggesting that this protein warrants investigation as a therapeutic target.

read more

Citations
More filters
Journal ArticleDOI

High mobility group box-1 protein in patients with suspected community-acquired infections and sepsis: a prospective study

TL;DR: In a cohort of patients with suspected community-acquired infections and sepsis, HMGB1 levels were statistically significantly higher in patients compared to the healthy controls, and there was no statistically significant difference between the infected and the non-infected patients.
Journal ArticleDOI

Plasma concentrations of high-mobility group box protein 1, soluble receptor for advanced glycation end-products and circulating DNA in patients with acute pancreatitis.

TL;DR: A complex study of the plasma levels of HMGB1, sRAGE and circulating DNA can be informative in evaluations of acute pancreatitis with different levels of severity.
Journal Article

Cholinergic modulation of inflammation.

TL;DR: This work has provided a rationale for exploring new possibilities to treat excessive, disease-underlying inflammation by applying selective cholinergic modalities in preclinical and clinical settings.
Journal ArticleDOI

Differential microRNA expression and virulence of avian, 1918 reassortant, and reconstructed 1918 influenza A viruses.

TL;DR: It is suggested that virulence of highly pathogenic influenza viruses may be mediated in part by cellular microRNA through dysregulation of genes critical to the inflammatory process.
Patent

Compositions and Methods of Altering Cholesterol Levels

TL;DR: In this article, the present invention relates to compositions, methods and kits using polynucleotides, primary transcripts and mmRNA molecules, and is related to the present paper.
References
More filters
Journal ArticleDOI

Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

TL;DR: The mammalian Tlr4 protein has been adapted primarily to subserve the recognition of LPS and presumably transduces the LPS signal across the plasma membrane.
Journal ArticleDOI

Shock and tissue injury induced by recombinant human cachectin.

TL;DR: It appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.
Journal ArticleDOI

Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia

TL;DR: Protection against shock, vital organ dysfunction, persistent stress hormone release and death was conferred by administration of antibodies 2 h before bacterial infusion, indicating that cachectin is a mediator of fatal bacteraemic shock and suggesting that antibodies against Cachectin offer a potential therapy of life-threatening infection.
Journal ArticleDOI

Detection of circulating tumor necrosis factor after endotoxin administration.

TL;DR: It is concluded that the response to endotoxin is associated with a brief pulse of circulating tumor necrosis factor and that the resultant responses are effected through the cyclooxygenase pathway.
Related Papers (5)