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Published ahead of print on September 16, 2004, doi:10.1164/rccm.200402-188OC

Am. J. Respir. Crit. Care Med., Volume 170, Number 12, December 2004, 1310-1316

A more recent version of this article appeared on December 15, 2004
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Submitted on February 18, 2004
Accepted on September 12, 2004

Contributions of High Mobility Group Box Protein in Experimental and Clinical Acute Lung Injury

Hiroshi Ueno1, Tomoyuki Matsuda1, Satoru Hashimoto1*, Fumimasa Amaya1, Yoshihiro Kitamura1, Masaki Tanaka2, Atsuko Kobayashi3, Ikuro Maruyama4, Shingo Yamada4, Naoki Hasegawa5, Junko Soejima5, Hidefumi Koh5, and Akitoshi Ishizaka5

1 Department of Anesthesiology and Intensive Care, Kyoto Prefectural University of Medicine, Kyoto, Japan, 2 Department of Anatomy, Kyoto Prefectural University of Medicine, Kyoto, Japan, 3 Intensive Care Unit, Saiseikai Suita Hospital, Osaka, Japan, 4 Department of Laboratory and Molecular Medicine, Kagoshima University, Faculty of Medicine, Kagoshima, Japan, 5 Department of Medicine, Keio University, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: satoru{at}koto.kpu-m.ac.jp.

This study was performed to examine the putative role of high-mobility group box (HMGB) protein in the pathogenesis of acute lung injury. Observations were made 1) in 21 septic patients with acute lung injury and 15 patients with normal lung function, and 2) in a mouse model, 24 h after intratracheal instillation of lipopolysaccharide. The concentrations of HMGB1 were increased in plasma and lung epithelial lining fluid of patients with acute lung injury and mice instilled with lipopolysaccharide. Lipopolysaccharide-induced acute lung injury was mitigated by anti-HMGB1 antibody. Although this protein was not detected in the plasma of control humans or mice, the concentrations of HMGB1 in lung epithelial lining fluid or in bronchoalveolar lavage fluid were unexpectedly high. The nuclear expression of HMGB1 was apparent in epithelial cells surrounding terminal bronchioles in normal mice, while its nuclear and cytoplasmic expression was observed in alveolar macrophages in lipopolysaccharide-instilled mice. Lung instillation of HMGB2 did not cause as much inflammation as HMGB1. Extracellular HMGB1 may play a key role in the pathogenesis of clinical and experimental acute lung injury. However, its expression in normal airways is noteworthy, and suggests that it also plays a physiologic role in the lung.
Key words: High mobility group box-1 protein, High mobility group box-2 protein, Acute respiratory distress syndrome Endotoxin, Lipopolysaccharide




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