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1 Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, USA; Department of Internal Medicine, Chung Ang University College of Medicine, Seoul, Korea, Republic of
2 Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, USA
3 Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, USA; Service d' Anesthesie-Reanimation et Unite Propre de Recherche de l' Enseignment Superieur-Equipe d'Accueil, Hospital de Bicetre, Le Kremlin Bicetre, France
4 Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, USA; Department of Anesthosiology, Chonnam University Medical School, Gwangju, Chonnam Province, Korea
5 Shino-Test Corporation, Central Institute, Sagamihara, Kanagawa, Japan
6 Department of Laboratory and Molecular Medicine, Faculty of Medicine, Kagoshima University, Kagoshima, Japan
7 Department of Medicine, Keio University, School of Medicine, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: Edward.Abraham{at}uchsc.edu.
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 hours of hemorrhage and then remained elevated for more than 72 hours after blood loss. Neutrophils appeared to contribute to the increase in post-hemorrhage 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 (KC), interleukin 6 (IL-6),
and interleukin-1
(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.
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