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Activation of the complement cascade by trypsin.

L Roxvall1, A Bengtson, L Sennerby

  • 1Dept. of Surgery, University of Gothenburg, Sweden.

Biological Chemistry Hoppe-Seyler
|April 1, 1991
PubMed
Summary
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Elevated plasma trypsin levels are common in acute pancreatitis. Trypsin activates complement, releasing anaphylatoxins and forming the terminal complement complex, which may contribute to disease severity.

Area of Science:

  • Biochemistry
  • Immunology
  • Gastroenterology

Background:

  • Acute pancreatitis is a serious condition with potential for systemic complications.
  • The role of trypsin in activating inflammatory pathways during pancreatitis requires further elucidation.

Purpose of the Study:

  • To investigate plasma immunoreactive trypsin levels in patients with acute pancreatitis.
  • To determine the effects of trypsin on complement activation and leukocyte function.

Main Methods:

  • Radioimmunoassay (RIA) for plasma immunoreactive trypsin, C3a, and C5a.
  • Enzyme-linked immunosorbent assay (ELISA) for terminal complement complex (TCC).
  • Chemiluminescence assay to assess leukocyte activation.

Main Results:

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  • All patient groups exhibited elevated plasma immunoreactive trypsin levels.
  • Bovine trypsin activated the complement cascade, leading to C3a and C5a release and TCC formation.
  • Trypsin-treated serum activated leukocytes, suggesting a role for complement split products.

Conclusions:

  • Trypsin can activate complement components in human serum.
  • Trypsin-induced complement activation generates anaphylatoxins and TCC, potentially mediating inflammatory effects in pancreatitis.
  • These findings support the hypothesis that trypsin contributes to the pathogenesis of acute pancreatitis through complement and leukocyte activation.