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Oxidative autoaggression by phagocytes in human peritonitis

A G Billing1, M Jochum, D Fröhlich

  • 1Chirurgische Klinik, Universität München, Klinikum Grosshadern, Munich, Germany.

European Journal of Clinical Investigation
|February 18, 1998
PubMed
Summary

Peritonitis causes significant inflammatory cell influx and high levels of oxidative enzymes like myeloperoxidase and elastase in abdominal exudates. This overwhelming phagocytic activity inactivates protective alpha 1-proteinase inhibitor, potentially damaging defense systems.

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Area of Science:

  • Biochemistry
  • Immunology
  • Cell Biology

Background:

  • Peritonitis is characterized by inflammation within the abdominal cavity.
  • Phagocytic cells play a crucial role in inflammatory responses.
  • Oxidative systems and proteases are key mediators of inflammation.

Purpose of the Study:

  • To investigate the levels of phagocyte-derived oxidative systems and proteases in abdominal exudates from peritonitis patients.
  • To compare inflammatory markers in purulent exudates versus clear exudates.

Main Methods:

  • Measurement of myeloperoxidase, chemiluminescence, and elastase in 60 abdominal exudates.
  • Analysis of inflammatory cell counts (leukocytes).
  • Assessment of alpha 1-proteinase inhibitor (alpha 1 PI) complexation and activity.

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Main Results:

  • Purulent exudates showed significantly higher leukocyte counts and 1000-fold increases in myeloperoxidase and elastase compared to normal plasma.
  • Chemiluminescence indicated dramatically increased phagocyte respiratory burst activity.
  • Active elastase was found in 60% of samples, with evidence of alpha 1 PI inactivation and degradation, unlike in clear exudates.

Conclusions:

  • Peritonitis leads to maximal inflammatory activation with overwhelming local phagocytic activity.
  • This activity results in protease inhibitor consumption and inactivation, likely due to oxidative destruction.
  • The potent oxidative environment in purulent exudates may compromise various host defense mechanisms.