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PMID: 17171797 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Blockade of high mobility group box-1 protein attenuates experimental severe acute pancreatitis.

World journal of gastroenterology ·Vol. 12 ·No. 47 ·2006-12-21 ·Pages 7666-70

Sawa H, Ueda T, Takeyama Y, Yasuda T, Shinzeki M, Nakajima T, Kuroda Y

Abstract

To examine the effects of anti-high mobility group box 1 (HMGB1) neutralizing antibody in experimental severe acute pancreatitis (SAP). 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 microg). Severity of pancreatitis, organ injury (liver, kidney and lung), and bacterial translocation to pancreas was examined 12 h after induction of SAP. 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. 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.

MeSH Terms
Animals Antibodies/pharmacology Female HMGB1 Protein/antagonists & inhibitors,immunology Immunotherapy/methods Mice Mice, Inbred C3H Pancreatitis/immunology,pathology,therapy Severity of Illness Index
Chemicals
Antibodies HMGB1 Protein
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Sawa Hidehiro
Department of Gastroenterological Surgery, Kobe University Graduate School of Medical Sciences, Kobe 650-0017, Japan. [email protected]
Ueda Takashi
Takeyama Yoshifumi
Yasuda Takeo
Shinzeki Makoto
Nakajima Takahiro
Kuroda Yoshikazu
References (35)
35 references, click to expand
  1. Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response.
    J Clin Invest. 2004 Jun;113(11):1641-50 PMID: 15173891
  2. Mini-review: The nuclear protein HMGB1 as a proinflammatory mediator.
    Eur J Immunol. 2004 Jun;34(6):1503-12 PMID: 15162419
  3. Bacterial contamination of pancreatic necrosis. A prospective clinical study.
    Gastroenterology. 1986 Aug;91(2):433-8 PMID: 3522342
  4. The role of the gut in the development of sepsis in acute pancreatitis.
    J Surg Res. 1991 Jul;51(1):18-23 PMID: 2067354
  5. Pathogenesis of pancreatic sepsis.
    Am J Surg. 1993 Jan;165(1):46-50; discussion 51-2 PMID: 8418702
  6. Bacterial translocation: a potential source for infection in acute pancreatitis.
    Pancreas. 1993 Sep;8(5):551-8 PMID: 8302791
  7. The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of rage and amphoterin in the developing nervous system.
    J Biol Chem. 1995 Oct 27;270(43):25752-61 PMID: 7592757
  8. A human homologue of the Drosophila Toll protein signals activation of adaptive immunity.
    Nature. 1997 Jul 24;388(6640):394-7 PMID: 9237759
  9. Relationship of necrosis to organ failure in severe acute pancreatitis.
    Gastroenterology. 1997 Sep;113(3):899-903 PMID: 9287982
  10. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene.
    Science. 1998 Dec 11;282(5396):2085-8 PMID: 9851930
  11. HMG-1 as a late mediator of endotoxin lethality in mice.
    Science. 1999 Jul 9;285(5425):248-51 PMID: 10398600
  12. Regulation of DNA-dependent activities by the functional motifs of the high-mobility-group chromosomal proteins.
    Mol Cell Biol. 1999 Aug;19(8):5237-46 PMID: 10409715
  13. Coregulatory proteins in steroid hormone receptor action: the role of chromatin high mobility group proteins HMG-1 and -2.
    Steroids. 1999 Sep;64(9):576-86 PMID: 10503712
  14. Contributions of high mobility group box protein in experimental and clinical acute lung injury.
    Am J Respir Crit Care Med. 2004 Dec 15;170(12):1310-6 PMID: 15374839
  15. Persistent elevation of high mobility group box-1 protein (HMGB1) in patients with severe sepsis and septic shock.
    Crit Care Med. 2005 Mar;33(3):564-73 PMID: 15753748
  16. The nuclear factor HMGB1 mediates hepatic injury after murine liver ischemia-reperfusion.
    J Exp Med. 2005 Apr 4;201(7):1135-43 PMID: 15795240
  17. High mobility group box 1 (HMGB1).
    Crit Care Med. 2005 Dec;33(12 Suppl):S472-4 PMID: 16340425
  18. Plasma concentrations and importance of High Mobility Group Box protein in the prognosis of organ failure in patients with disseminated intravascular coagulation.
    Thromb Haemost. 2005 Nov;94(5):975-9 PMID: 16363239
  19. Contribution of high-mobility group box-1 to the development of ventilator-induced lung injury.
    Am J Respir Crit Care Med. 2006 Aug 15;174(4):400-7 PMID: 16728713
  20. Anti-high-mobility group box chromosomal protein 1 antibodies improve survival of rats with sepsis.
    World J Surg. 2006 Sep;30(9):1755-62 PMID: 16850155
  21. Significant increase of serum high-mobility group box chromosomal protein 1 levels in patients with severe acute pancreatitis.
    Pancreas. 2006 Nov;33(4):359-63 PMID: 17079940
  22. Increased serum concentrations of high-mobility-group protein 1 in haemorrhagic shock.
    Lancet. 1999 Oct 23;354(9188):1446-7 PMID: 10543678
  23. HMG-1 as a mediator of acute lung inflammation.
    J Immunol. 2000 Sep 15;165(6):2950-4 PMID: 10975801
  24. Acute necrotizing pancreatitis: treatment strategy according to the status of infection.
    Ann Surg. 2000 Nov;232(5):619-26 PMID: 11066131
  25. High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes.
    J Exp Med. 2000 Aug 21;192(4):565-70 PMID: 10952726
  26. Dynamic nature of early organ dysfunction determines outcome in acute pancreatitis.
    Br J Surg. 2002 Mar;89(3):298-302 PMID: 11872053
  27. The significance of changes in high mobility group-1 protein mRNA expression in rats after thermal injury.
    Shock. 2002 Apr;17(4):329-33 PMID: 11954836
  28. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation.
    Nature. 2002 Jul 11;418(6894):191-5 PMID: 12110890
  29. HMGB1 B box increases the permeability of Caco-2 enterocytic monolayers and impairs intestinal barrier function in mice.
    Gastroenterology. 2002 Sep;123(3):790-802 PMID: 12198705
  30. High mobility group box chromosomal protein 1 plays a role in the pathogenesis of rheumatoid arthritis as a novel cytokine.
    Arthritis Rheum. 2003 Apr;48(4):971-81 PMID: 12687539
  31. High mobility group protein 1 (HMGB1) quantified by ELISA with a monoclonal antibody that does not cross-react with HMGB2.
    Clin Chem. 2003 Sep;49(9):1535-7 PMID: 12928240
  32. Further characterization of high mobility group box 1 (HMGB1) as a proinflammatory cytokine: central nervous system effects.
    Cytokine. 2003 Dec 21;24(6):254-65 PMID: 14609567
  33. Reversing established sepsis with antagonists of endogenous high-mobility group box 1.
    Proc Natl Acad Sci U S A. 2004 Jan 6;101(1):296-301 PMID: 14695889
  34. Involvement of toll-like receptors 2 and 4 in cellular activation by high mobility group box 1 protein.
    J Biol Chem. 2004 Feb 27;279(9):7370-7 PMID: 14660645
  35. A new group of chromatin-associated proteins with a high content of acidic and basic amino acids.
    Eur J Biochem. 1973 Sep 21;38(1):14-9 PMID: 4774120
Article Info
Journal
World journal of gastroenterology
Abbr.
World J Gastroenterol
ISSN
1007-9327
Published
2006-12-21
Pages
7666-70
Language
English
Region
United States
NLM ID
100883448
PMCID
PMC4088050
Subset
IM
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