Lymphocyte subsets and cytokines in ascitic fluid of decompensated cirrhotic patients with and without spontaneous ascites infection

Background and Aim: Spontaneous ascites infection is a frequently encountered and important complication of decompensated liver cirrhosis. The immune system plays an important role in the development or eradication of this infection. A number of compositional and functional alterations in immune system cells have been demonstrated in cirrhotic patients; however, there is a lack of knowledge about this issue in ascitic infections. The aim of the present study was to evaluate lymphocyte subsets and levels of some ascitic and lymphocytic intracytoplasmic cytokines in decompensated cirrhotic patients with or without spontaneous ascites infection. Methods: The study population consisted of 45 decompensated cirrhotic patients (32 men, 13 women) with different etiologies. Patients with ascitic polymorphonuclear leukocyte count ≥250/mm3 and/or positive ascitic bacterial cultures were classified as the ‘infected group’. Comparison was made between the infected and non‐infected group for the following parameters: ascites leukocyte counts and differentiations; ascitic fluid protein; albumin levels and serum‐ascites albumin gradients; flow cytometric detection of cell surface markers for ascitic T, B and natural killer lymphocytes; intracytoplasmic interleukin (IL)‐2, IL‐4, tumor necrosis factor (TNF)‐α and interferon (IFN)‐γ; levels of ascitic IL‐8, IL‐10, IL‐12 and TNF‐α; and soluble Fas antigen and soluble Fas ligand. Results: The CD4/CD8 ratio was significantly decreased and expression of T cell receptor‐γδ was increased in the infected group. Furthermore, ascites TNF‐α levels were also elevated in this group. Ascitic IL‐8, IL‐10, IL‐12 and TNF‐α levels were significantly higher in patients with positive ascitic bacterial culture. Conclusions: These results suggest that a cytotoxic, especially Th1, immune response predominates in ascites infections. It also demonstrates that TNF‐α might be involved in the pathogenesis of ascites infections.