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Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Dec 21, 2006; 12(47): 7666-7670
Published online Dec 21, 2006. doi: 10.3748/wjg.v12.i47.7666
Blockade of high mobility group box-1 protein attenuates experimental severe acute pancreatitis
Hidehiro Sawa, Takashi Ueda, Yoshifumi Takeyama, Takeo Yasuda, Makoto Shinzeki, Takahiro Nakajima, Yoshikazu Kuroda
Hidehiro Sawa, Takashi Ueda, Takeo Yasuda, Makoto Shinzeki, Takahiro Nakajima, Yoshikazu Kuroda, Department of Gastroenterological Surgery, Kobe University Graduate School of Medical Sciences, Kobe 650-0017, Japan
Yoshifumi Takeyama, Department of Surgery, Kinki University School of Medicine, Osaka-sayama 589-8511, Japan
Author contributions: All authors contributed equally to the work.
Supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan and from the Ministry of Health, Labor and Welfare of Japan
Correspondence to: Hidehiro Sawa, Department of Gastroente-rological Surgery, Kobe University Graduate School of Medical Sciences, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan. hdhrsawa@med.kobe-u.ac.jp
Telephone: +81-78-3825925 Fax: +81-78-3825939
Received: October 17, 2006
Revised: November 10, 2006
Accepted: November 20, 2006
Published online: December 21, 2006
Abstract

AIM: To examine the effects of anti-high mobility group box 1 (HMGB1) neutralizing antibody in experimental severe acute pancreatitis (SAP).

METHODS: SAP was induced by creating closed duodenal loop in C3H/HeN mice. SAP was induced immediately after intraperitoneal injection of anti-HMGB1 neutralizing antibody (200 μg). Severity of pancreatitis, organ injury (liver, kidney and lung), and bacterial translocation to pancreas was examined 12 h after induction of SAP.

RESULTS: Anti-HMGB1 neutralizing antibody significantly improved the elevation of the serum amylase level and the histological alterations of pancreas and lung in SAP. Anti-HMGB1 antibody also significantly ameliorated the elevations of serum alanine aminotransferase and creatinine in SAP. However, anti-HMGB1 antibody worsened the bacterial translocation to pancreas.

CONCLUSION: Blockade of HMGB1 attenuated the development of SAP and associated organ dysfunction, suggesting that HMGB1 may act as a key mediator for inflammatory response and organ injury in SAP.

Keywords: Severe acute pancreatitis, High mobility group box-1, Neutralizing antibody, Inflammatory response, Organ dysfunction, Bacterial translocation