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[Functions of circulating and intra-abdominal polymorphonuclear leukocytes during human secondary peritonitis]
K Holzer1, A Richter, P Konietzny
1Klinik für Allgemein- und Gefässchirurgie, Universitä tsklinik Frankfurt/Main.
Introduction:
Aim of the study was to characterize different functions of circulating and emigrated, intra-abdominal polymorphonuclear leukocytes (cPMNs, ePMNs) during human secondary peritonitis.
Methods:
In patients (n=25) with diffuse secondary peritonitis circulating and emigrated PMNs were characterized intra- and until 96 h postoperatively. Patients were allocated to two different groups, e. g. patients with septic complications (shock, organ failure, n=11) and patients without complications (n=14) during peritonitis. In addition a control group of patients (n=10) with abdominal surgery but without peritonitis was investigated. The lucigenin- and luminol-enhanced chemiluminescence was used to determine extra- and intracellular oxygen radical generation of PMNs. Besides spontaneous oxygen radical generation of PMNs, stimulated radical production was investigated after the addition of ionophores A23 187 and C3-coated zymosan. Phagocytosis by PMNs was characterized with opsonized E. coli bacteria and fluorescence-activated cell analysis.
Results:
Especially patients with complicated peritonitis had strong and long-lasting changes of PMNs functions. The toxic and tissue-destroying production of extracellular oxygen radicals by circulating PMNs was enhanced (e. g., A23 187 - stimulated oxygen radical generation 433 +/- 89 cpm/cPMNs (peritonitis with complications) versus 90 +/- 30 cpm/cPMNs (peritonitis without complications) versus 110 +/- 44 cpm/cPMNs (controls), p < 0.05). Phagocytosis (58 +/- 9 % (ePMNs, peritonitis with complications) versus 81 +/- 6 % (ePMNs, peritonitis without complications) versus 82.2 +/- 1.6 % (ePMNs, controls), p < 0.05) and phagocytosis-associated intracellular oxygen radical generation (8.23 +/- 1.6 x 10(3) cpm/ePMNs (peritonitis with complications) versus 25.2 +/- 5.2 x 10(3) cpm/ePMNs (peritonitis without complications) versus 11.7 +/- 2.8 cpm x 10(3) cpm/ePMNs (controls) p < 0.05) were suppressed.
Conclusion:
Not for all patients with peritonitis does it seem favourable to modulate PMNs-functions. If immunomodulation would be able to down-regulate exaggerated functions of circulating PMNs and to up-regulate the suppressed functions of emigrated PMNs patients with complicated peritonitis might benefit from this therapy.
Insights
Polymorphonuclear leukocytes (PMNs) show altered functions in secondary peritonitis. Complicated peritonitis impairs phagocytosis and increases harmful radical production, suggesting targeted immunomodulation could benefit patients.
Area of Science:
- Immunology
- Cell Biology
- Sepsis Research
Context:
- Secondary peritonitis involves intra-abdominal inflammation and potential sepsis.
- Polymorphonuclear leukocytes (PMNs) are critical immune cells involved in fighting infection.
- Characterizing PMN function is vital for understanding peritonitis pathogenesis and outcomes.
Purpose:
- To characterize the functions of circulating and emigrated PMNs in patients with secondary peritonitis.
- To compare PMN functions between patients with complicated and uncomplicated peritonitis.
- To investigate the role of PMN oxygen radical generation and phagocytosis.
Summary:
- Patients with complicated peritonitis exhibited enhanced extracellular oxygen radical production by circulating PMNs.
- Phagocytosis and associated intracellular oxygen radical generation by emigrated PMNs were suppressed in complicated peritonitis.
- PMN function was significantly altered in patients with septic complications compared to those without.
Impact:
- Findings suggest that PMN function is significantly impaired in severe secondary peritonitis.
- Altered PMN functions, including suppressed phagocytosis and increased radical production, correlate with septic complications.
- This research highlights potential therapeutic targets for immunomodulation in peritonitis management.