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Changes in the production of nitric oxide and superoxide by inflammatory cells in liver cirrhosis

E Masini1, L Mugnai, M Foschi

  • 1Department of Preclinical and Clinical Pharmacology, University of Flourence, Italy.

International Archives of Allergy and Immunology
|May 1, 1995
PubMed

Insights

Liver cirrhosis patients show altered inflammatory cell function. Polymorphonuclear leukocytes (PMNs) produce less superoxide but more nitric oxide (NO), indicating a shift in immune response related to liver disease.

Area of Science:

  • Immunology
  • Hepatology
  • Cellular Biology

Background:

  • Liver cirrhosis is associated with systemic inflammation and altered immune cell function.
  • Polymorphonuclear leukocytes (PMNs) and monocytes play critical roles in innate immunity and inflammation.
  • Understanding immune cell responses in cirrhosis is crucial for managing complications.

Purpose of the Study:

  • To evaluate superoxide (O2-) and nitric oxide (NO) production by PMNs and monocytes in patients with liver cirrhosis.
  • To investigate the activity of NO synthase in leukocytes from cirrhotic patients.
  • To explore correlations between inflammatory cell changes and hemodynamic parameters like cardiac index.

Main Methods:

  • Isolation of PMNs and monocytes from cirrhotic patients and healthy controls.
  • Stimulation of leukocytes with opsonized zymosan to assess O2- production.
  • Measurement of NO production through inhibition of platelet aggregation and cGMP content analysis.
  • Assay of NO synthase activity in leukocyte extracts.
  • Correlation analysis between cellular function and cardiac index.

Main Results:

  • PMNs from cirrhotic patients exhibited reduced O2- production compared to controls.
  • Leukocytes from cirrhotic patients demonstrated enhanced NO production, evidenced by platelet aggregation inhibition and increased cGMP.
  • Higher NO synthase activity was observed in leukocytes of cirrhotic patients.
  • A significant correlation was found between the cardiac index and alterations in inflammatory cell function.

Conclusions:

  • Immune cell dysfunction, specifically reduced O2- and increased NO production by PMNs, is characteristic of liver cirrhosis.
  • Elevated NO synthase activity contributes to the altered inflammatory profile in cirrhotic patients.
  • These immune cell changes may be linked to hemodynamic alterations, suggesting a complex interplay in the pathophysiology of liver cirrhosis.

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