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Science 9 July 1999:
Vol. 285. no. 5425, pp. 248 - 251
DOI: 10.1126/science.285.5425.248
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Reports

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

Haichao Wang, 13* Ona Bloom, 3 Minghuang Zhang, 3 Jaideep M. Vishnubhakat, 3 Michael Ombrellino, 23 Jiantu Che, 3 Asia Frazier, 23 Huan Yang, 3 Svetlana Ivanova, 3 Lyudmila Borovikova, 3 Kirk R. Manogue, 3 Eugen Faist, 4 Edward Abraham, 5 Jan Andersson, 6 Ulf Andersson, 7 Patricia E. Molina, 2 Naji N. Abumrad, 2 Andrew Sama, 1 Kevin J. Tracey 23

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.

1 Department of Emergency Medicine and
2 Department of Surgery, North Shore University Hospital-New York University School of Medicine, Manhasset, NY 11030, USA.
3 The Picower Institute for Medical Research, Manhasset, NY 11030, USA.
4 Department of Surgery, Klinicum Grosshadern, Ludwig-Maximilians University, Munich, Germany.
5 Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
6 Department of Infectious Disease, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden.
7 Department of Rheumatology, Astrid Lindgren's Children's Hospital, Karolinska Institute, Stockholm, Sweden.
*   To whom correspondence should be addressed. E-mail: hwang{at}picower.edu

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   Abstract »    Full Text »    PDF »
Hemorrhagic Shock Induces NAD(P)H Oxidase Activation in Neutrophils: Role of HMGB1-TLR4 Signaling.
J. Fan, Y. Li, R. M. Levy, J. J. Fan, D. J. Hackam, Y. Vodovotz, H. Yang, K. J. Tracey, T. R. Billiar, and M. A. Wilson (2007)
J. Immunol. 178, 6573-6580
   Abstract »    Full Text »    PDF »
Masquerader: High Mobility Group Box-1 and Cancer.
J. E. Ellerman, C. K. Brown, M. de Vera, H. J. Zeh, T. Billiar, A. Rubartelli, and M. T. Lotze (2007)
Clin. Cancer Res. 13, 2836-2848
   Abstract »    Full Text »    PDF »
Pathophysiology of Sepsis.
D. G. Remick (2007)
Am. J. Pathol. 170, 1435-1444
   Abstract »    Full Text »    PDF »
A Cardiovascular Drug Rescues Mice from Lethal Sepsis by Selectively Attenuating a Late-Acting Proinflammatory Mediator, High Mobility Group Box 1.
W. Li, J. Li, M. Ashok, R. Wu, D. Chen, L. Yang, H. Yang, K. J. Tracey, P. Wang, A. E. Sama, et al. (2007)
J. Immunol. 178, 3856-3864
   Abstract »    Full Text »    PDF »
Cellular Mechanisms in Sepsis.
E. Jean-Baptiste (2007)
J Intensive Care Med 22, 63-72
   Abstract »    PDF »
Hydrogen peroxide stimulates macrophages and monocytes to actively release HMGB1.
D. Tang, Y. Shi, R. Kang, T. Li, W. Xiao, H. Wang, and X. Xiao (2007)
J. Leukoc. Biol. 81, 741-747
   Abstract »    Full Text »    PDF »
IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factor in vivo.
V. Carriere, L. Roussel, N. Ortega, D.-A. Lacorre, L. Americh, L. Aguilar, G. Bouche, and J.-P. Girard (2007)
PNAS 104, 282-287
   Abstract »    Full Text »    PDF »
Pivotal Advances: High-mobility group box 1 protein--a cytokine with a role in cardiac repair.
A. Germani, F. Limana, and M. C. Capogrossi (2007)
J. Leukoc. Biol. 81, 41-45
   Abstract »    Full Text »    PDF »
High mobility group box-1 protein induces the migration and activation of human dendritic cells and acts as an alarmin.
D. Yang, Q. Chen, H. Yang, K. J. Tracey, M. Bustin, and J. J. Oppenheim (2007)
J. Leukoc. Biol. 81, 59-66
   Abstract »    Full Text »    PDF »
Cytolytic cells induce HMGB1 release from melanoma cell lines.
N. Ito, R. A. DeMarco, R. B. Mailliard, J. Han, H. Rabinowich, P. Kalinski, D. B. Stolz, H. J. Zeh III, and M. T. Lotze (2007)
J. Leukoc. Biol. 81, 75-83
   Abstract »    Full Text »    PDF »
Analysis of proinflammatory activity of highly purified eukaryotic recombinant HMGB1 (amphoterin).
A. Rouhiainen, S. Tumova, L. Valmu, N. Kalkkinen, and H. Rauvala (2007)
J. Leukoc. Biol. 81, 49-58
   Abstract »    Full Text »    PDF »
The maturation potential of NK cell clones toward autologous dendritic cells correlates with HMGB1 secretion.
C. Semino, J. Ceccarelli, L. V. Lotti, M. R. Torrisi, G. Angelini, and A. Rubartelli (2007)
J. Leukoc. Biol. 81, 92-99
   Abstract »    Full Text »    PDF »
Interview with Dr. Heikki Rauvala regarding Pivotal Advance: Analysis of proinflammatory activity of highly purified eukaryotic recombinant HMGB1 (amphoterin).
M. E. Bianchi (2007)
J. Leukoc. Biol. 81, 46-48
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Factors masking HMGB1 in human serum and plasma.
V. Urbonaviciute, B. G. Furnrohr, C. Weber, M. Haslbeck, S. Wilhelm, M. Herrmann, and R. E. Voll (2007)
J. Leukoc. Biol. 81, 67-74
   Abstract »    Full Text »    PDF »
Treatment with HMGB1 inhibitors diminishes CTL-induced liver disease in HBV transgenic mice.
G. Sitia, M. Iannacone, S. Muller, M. E. Bianchi, and L. G. Guidotti (2007)
J. Leukoc. Biol. 81, 100-107
   Abstract »    Full Text »    PDF »
HMGB1-secreting capacity of multiple cell lineages revealed by a novel HMGB1 ELISPOT assay.
H. Wahamaa, T. Vallerskog, S. Qin, C. Lunderius, G. LaRosa, U. Andersson, and H. E. Harris (2007)
J. Leukoc. Biol. 81, 129-136
   Abstract »    Full Text »    PDF »
Increasing numbers of hepatic dendritic cells promote HMGB1-mediated ischemia-reperfusion injury.
A. Tsung, N. Zheng, G. Jeyabalan, K. Izuishi, J. R. Klune, D. A. Geller, M. T. Lotze, L. Lu, and T. R. Billiar (2007)
J. Leukoc. Biol. 81, 119-128
   Abstract »    Full Text »    PDF »


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