Gradual Increase of High Mobility Group Protein B1 in the Lungs after the Onset of Acute Exacerbation of Idiopathic Pulmonary FibrosisReport as inadecuate

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Pulmonary MedicineVolume 2011 2011, Article ID 916486, 9 pages

Research Article

Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, 1-1 Seiryo, Aoba-ku, Sendai 980-8574, Japan

Department of Respiratory Medicine, Tosei General Hospital, Seto, Aichi 489-8642, Japan

Department of Veterinary Biochemistry, Rakuno Gakuen University, Ebetsu, Hokkaido 069-8501, Japan

Central Institute, Shino-Test Corporation, Kanagawa 229-0011, Japan

Virus Research Center, National Hospital Organization, Sendai 983-0045, Japan

Department of Medicine, Keio University, Tokyo 160-8582, Japan

Department of Laboratory and Molecular Medicine, Kagoshima University, Kagoshima 890-8520, Japan

Department of Thoracic Surgery, Tohoku University Hospital, Sendai 980-8574, Japan

Received 14 August 2010; Revised 27 December 2010; Accepted 29 December 2010

Academic Editor: A. Azuma

Copyright © 2011 Masahito Ebina et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The pathogenesis of acute exacerbation of idiopathic pulmonary fibrosis IPF remains to be elucidated. To evaluate the roles of inflammatory mediators in acute exacerbation, the concentrations of high mobility group protein B1 HMGB1, a chief mediator of acute lung injury, and 18 inflammatory cytokines were measured in the bronchoalveolar lavage fluid, serially sampled from seven IPF patients after the onset of acute exacerbation. HMGB1 gradually increased in the alveolar fluid after the onset of acute exacerbation, in positive correlation with monocytes chemotactic protein-1 MCP-1, a potent fibrogenic mediator. In the lung tissues of eight IPF patients autopsied after acute exacerbation, intense cytoplasmic staining for HMGB1 was observed in the alveolar epithelial cells in alveolar capillary augmented lesions, where the capillary endothelial cells remarkably reduced the expression of thrombomodulin, an intrinsic antagonist of HMGB1. These results suggest pathogenic roles for HMGB1 and MCP-1 in the late phase of acute exacerbation of IPF.

Author: Masahito Ebina, Hiroyuki Taniguchi, Taku Miyasho, Shingo Yamada, Naoko Shibata, Hiromitsu Ohta, Shu Hisata, Shinya Ohkouchi



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