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Research ArticleORIGINAL ARTICLE

Urinary Trypsin Inhibitor Protects against Systemic Inflammation Induced by Lipopolysaccharide

Ken-Ichiro Inoue, Hirohisa Takano, Akinori Shimada, Rie Yanagisawa, Miho Sakurai, Shin Yoshino, Hiroyuki Sato and Toshikazu Yoshikawa
Molecular Pharmacology March 2005, 67 (3) 673-680; DOI: https://doi.org/10.1124/mol.104.005967
Ken-Ichiro Inoue
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Hirohisa Takano
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Akinori Shimada
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Rie Yanagisawa
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Miho Sakurai
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Shin Yoshino
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Hiroyuki Sato
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Toshikazu Yoshikawa
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Abstract

Urinary trypsin inhibitor (UTI), a serine protease inhibitor, has been widely used as a drug for patients with acute inflammatory disorders such as disseminated intravascular coagulation, shock, and pancreatitis in Japan. Recent studies have demonstrated that serine protease inhibitors may play an anti-inflammatory role beyond merely an inhibitory action on neutrophil elastase at the site of inflammation at least in vitro. To clarify the direct contributions of UTI to inflammatory condition in vivo, we analyzed its roles in experimental systemic inflammatory response induced by intraperitoneal administration of lipopolysaccharide (LPS) using UTI deficient (–/–) mice and corresponding wild-type (WT) mice. After LPS (1 mg/kg) challenge, UTI (–/–) mice revealed a significant elevation of plasma fibrinogen and fibrinogen/fibrin degradation products and a decrease in white blood cell counts compared with WT mice. LPS treatment induced more severe neutrophilic inflammation in the lung and the kidney obtained from UTI (–/–) mice than in those from WT mice, which was confirmed by histological examination. The protein levels of proinflammatory mediators, such as macrophage chemoattractant protein (MCP)-1 in the lungs, MCP-1 and keratinocyte chemoattractant (KC) in the kidneys, and interleukin-1β, macrophage inflammatory protein-2, MCP-1, and KC in the liver, were significantly greater in UTI (–/–) mice than in WT mice after LPS challenge. Our results suggest that UTI protects against systemic inflammatory response and subsequent organ injury induced by bacterial endotoxin, at least partly through the inhibition of the enhanced expression of proinflammatory cytokines and chemokines.

  • Received August 8, 2004.
  • Accepted December 2, 2004.
  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 67 (3)
Molecular Pharmacology
Vol. 67, Issue 3
1 Mar 2005
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Research ArticleORIGINAL ARTICLE

Urinary Trypsin Inhibitor Protects against Systemic Inflammation Induced by Lipopolysaccharide

Ken-Ichiro Inoue, Hirohisa Takano, Akinori Shimada, Rie Yanagisawa, Miho Sakurai, Shin Yoshino, Hiroyuki Sato and Toshikazu Yoshikawa
Molecular Pharmacology March 1, 2005, 67 (3) 673-680; DOI: https://doi.org/10.1124/mol.104.005967

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Research ArticleORIGINAL ARTICLE

Urinary Trypsin Inhibitor Protects against Systemic Inflammation Induced by Lipopolysaccharide

Ken-Ichiro Inoue, Hirohisa Takano, Akinori Shimada, Rie Yanagisawa, Miho Sakurai, Shin Yoshino, Hiroyuki Sato and Toshikazu Yoshikawa
Molecular Pharmacology March 1, 2005, 67 (3) 673-680; DOI: https://doi.org/10.1124/mol.104.005967
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