HMG-1 as a late mediator of endotoxin lethality in mice.

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ID: 281480
1999
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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.
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wang1999hmg1 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Haichao Wang; O. Bloom; Minghuang Zhang; J. Vishnubhakat; Michael Ombrellino; J. Che; A. Frazier; Huan Yang; S. Ivanova; L. V. Borovikova; K. Manogue; E. Faist; E. Abraham; J. Andersson; U. Andersson; P. Molina; N. Abumrad; A. Sama; K. Tracey
Journal Science
Year 1999
DOI
10.1126/SCIENCE.285.5425.248
URL
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