| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, Colorado 2Central Institute, Shino-Test Corporation, Sagamihara, Kanagawa, Japan 3Department of Laboratory and Molecular Medicine, Faculty of Medicine, Kagoshima University, Kagoshima, Japan 4Department of Medicine, Keio University, School of Medicine, Tokyo, Japan 5Department of Internal Medicine, Chung Ang University College of Medicine, Seoul, Korea 6Service d'Anesthesie-Réanimation et Unité Propre de Recherche de l'Enseignment Superieur-Equipe d'Accueil, Hospital de Bicêtre, Le Kremlin Bicetre, France 7Department of Anesthesiology, Chonnam University Medical School, Gwangju, Korea
Submitted 21 September 2004 ; accepted in final form 3 January 2005
High mobility group box 1 (HMGB1) is a novel late mediator of inflammatory responses that contributes to endotoxin-induced acute lung injury and sepsis-associated lethality. Although acute lung injury is a frequent complication of severe blood loss, the contribution of HMGB1 to organ system dysfunction in this setting has not been investigated. In this study, HMGB1 was detected in pulmonary endothelial cells and macrophages under baseline conditions. After hemorrhage, in addition to positively staining endothelial cells and macrophages, neutrophils expressing HMGB1 were present in the lungs. HMGB1 expression in the lung was found to be increased within 4 h of hemorrhage and then remained elevated for more than 72 h after blood loss. Neutrophils appeared to contribute to the increase in posthemorrhage pulmonary HMGB1 expression since no change in lung HMGB1 levels was found after hemorrhage in mice made neutropenic with cyclophosphamide. Plasma concentrations of HMGB1 also increased after hemorrhage. Blockade of HMGB1 by administration of anti-HMGB1 antibodies prevented hemorrhage-induced increases in nuclear translocation of NF-
B in the lungs and pulmonary levels of proinflammatory cytokines, including keratinocyte-derived chemokine, IL-6, and IL-1
. Similarly, both the accumulation of neutrophils in the lung as well as enhanced lung permeability were reduced when anti-HMGB1 antibodies were injected after hemorrhage. These results demonstrate that hemorrhage results in increased HMGB1 expression in the lungs, primarily through neutrophil sources, and that HMGB1 participates in hemorrhage-induced acute lung injury.
high mobility group box 1; nuclear factor-B; neutrophils
This article has been cited by other articles:
|
|
 |
|
  T. Kohno, T. Anzai, K. Naito, T. Miyasho, M. Okamoto, H. Yokota, S. Yamada, Y. Maekawa, T. Takahashi, T. Yoshikawa, et al. Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodelling Cardiovasc Res, December 2, 2008; (2008) cvn291v2. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Tajima, M. Kohno, M. Watanabe, Y. Izumi, S. Tasaka, I. Maruyama, T. Miyasho, and K. Kobayashi Occult injury in the residual lung after pneumonectomy in mice Interactive CardioVascular and Thoracic Surgery, December 1, 2008; 7(6): 1114 - 1120. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Rowe, P. L. Jackson, G. Liu, M. Hardison, A. Livraghi, G. M. Solomon, D. B. McQuaid, B. D. Noerager, A. Gaggar, J. P. Clancy, et al. Potential Role of High-Mobility Group Box 1 in Cystic Fibrosis Airway Disease Am. J. Respir. Crit. Care Med., October 15, 2008; 178(8): 822 - 831. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H.-P. Tzeng, J. Fan, J. G. Vallejo, J. W. Dong, X. Chen, S. R. Houser, and D. L. Mann Negative inotropic effects of high-mobility group box 1 protein in isolated contracting cardiac myocytes Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1490 - H1496. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Levy, K. P. Mollen, J. M. Prince, D. J. Kaczorowski, R. Vallabhaneni, S. Liu, K. J. Tracey, M. T. Lotze, D. J. Hackam, M. P. Fink, et al. Systemic inflammation and remote organ injury following trauma require HMGB1 Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2007; 293(4): R1538 - R1544. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. M. Levy, J. M. Prince, R. Yang, K. P. Mollen, H. Liao, G. A. Watson, M. P. Fink, Y. Vodovotz, and T. R. Billiar Systemic inflammation and remote organ damage following bilateral femur fracture requires Toll-like receptor 4 Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2006; 291(4): R970 - R976. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. N. Ogawa, A. Ishizaka, S. Tasaka, H. Koh, H. Ueno, F. Amaya, M. Ebina, S. Yamada, Y. Funakoshi, J. Soejima, et al. Contribution of High-Mobility Group Box-1 to the Development of Ventilator-induced Lung Injury Am. J. Respir. Crit. Care Med., August 15, 2006; 174(4): 400 - 407. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Liu, D. B. Stolz, P. L. Sappington, C. A. Macias, M. E. Killeen, J. J. Tenhunen, R. L. Delude, and M. P. Fink HMGB1 is secreted by immunostimulated enterocytes and contributes to cytomix-induced hyperpermeability of Caco-2 monolayers Am J Physiol Cell Physiol, April 1, 2006; 290(4): C990 - C999. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Fan, Y. Li, Y. Vodovotz, T. R. Billiar, and M. A. Wilson Hemorrhagic shock-activated neutrophils augment TLR4 signaling-induced TLR2 upregulation in alveolar macrophages: role in hemorrhage-primed lung inflammation Am J Physiol Lung Cell Mol Physiol, April 1, 2006; 290(4): L738 - L746. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Lin, H. Yang, T. Sakuragi, M. Hu, L. L. Mantell, S. Hayashi, Y. Al-Abed, K. J. Tracey, L. Ulloa, and E. J. Miller {alpha}-Chemokine receptor blockade reduces high mobility group box 1 protein-induced lung inflammation and injury and improves survival in sepsis Am J Physiol Lung Cell Mol Physiol, October 1, 2005; 289(4): L583 - L590. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
