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A potential role for nitric oxide pathway in tuberculous pleural effusion
1Department of Biochemistry, School of Medicine, Ankara University, Sihhiye, Ankara, Turkey. elgun@medicine.ankara.edu.tr
Setting:
Tuberculous pleural effusion leads to an immune response involving mainly immune and mesothelial cells. Nitric oxide (NO) produced by these cells may have antimycobacterial effects against Mycobacterium tuberculosis.
Objective:
To investigate the possible role of NO in connection with the arginase enzyme, which controls the synthesis of NO through arginine depletion.
Design:
Pleural fluid samples from 20 patients with tuberculous pleural effusion were used for arginase activity and NO level determination. Results were compared with those from 12 lung cancer, 12 pneumonia and 12 congestive heart failure (CHF) patients.
Results:
Pleural arginase activity in tuberculosis patients was found to be significantly decreased compared to lung cancer and pneumonia groups, while the NO level was higher in tuberculosis patients. All groups except the CHF group had significant correlations between NO level and white blood cell count. Arginase activity and red blood cell count correlated significantly in lung cancer and CHF groups.
Conclusion:
The arginine-NO pathway seems to be involved in the pathogenesis of tuberculous pleural effusion. Decreased arginase activity may cause arginine accumulation, which may then lead to increased NO synthesis by immune and mesothelial cells, reflecting a host defence mechanism.