The pathogenesis of cytokines in preportal fibrosis of human infected with schistosomiasis and viral hepatitis

Cytokines are polypeptides exhibiting a variety of biological activities including metabolic, inflammatory, hematopoietic and immunologic properties.They play an important role in the pathogenesis of various diseases. Inflammation is commonly observed in liver diseases and is frequently complicated by fibrosis and cirrhosis in end-stage disease. The only curative treatment for cirrhotic patients is liver transplantation. Cytokines play a key role in the regulation of immune responses. In viral hepatitis the production of inappropriate cytokine level appears to contribute to viral persistence and to affect response to therapy. The aim of this study is to investigate the level of endogenous IL-1B, IL-6 and IL-10 to determine their relation with liver fibrosis. Forty patients with chronic liver disease and 10 normal adults as control group were studied. Patients in this study were classified into four groups according to etiology of chronic liver disease: Group I (10 patients with bilharzial liver disease),Group II (10 patients with chronic hepatitisC), Group III(10 patients with chronic hepatitisB )and Group IV (10 patients with chronic hepatitis B and C) . All patients with chronic liver disease (n=40) showed highly significant elevation of serum IL-1B, IL-6, IL-10 mean ± SD were (106.4±47.8) (P<0.01) (26.3 ±11.1) (P<0.01) (135.4± 73.9) (P<0.01) respectively when compared to control group. After classifying the patients into 4 groups each group showed highly significant elevation of serum IL-1B, serum IL-6 and serum IL-10 in each group when compared to control group( p < 5051). Regression analysis showed negative significant correlation between serum IL-10 and IL- 1B (r=-0.64, P<0.05), highly negative significant correlation between IL-10 and IL-6 (r=-0.72, P<0.01) in all patients with chronic liver diseases, also there was highly significant positive correlation between serum IL-1B and serum IL-6 (r=0.83, P<0.01). Ten patients with bilharzial liver disease (group I) showed highly negative significant correlation between serum IL-10 and each of serum IL-1B and serum IL-6 (r=-0.9, P<0.01) (r=- 0.8, P<0.01) respectively, and there was highly significant positive correlation between serum IL-1B and serum IL-6 (r=0.96, P<0.01) . There was significant correlation between prothrombin concentration and each of serum IL-10, serum IL-1B and IL-6 (r=0.7, P<0.05), (r=0.68, P<0.05), (r=0.74, P<0.05) respectively. Ten patients with chronic hepatitis C virus (group II) also showed highly negative significant correlation between serum IL-10 and each of serum IL-1B and serum IL-6 (r=-0.9, P<0.01) (r=-0.9, P<0.01) respectively. There was highly significant positive correlation between serum IL-1B and serum IL-6 (r=0.83, P<0.01) and significant correlation between serum IL-1B and serum ALT(r=0.63, P<0.05). As regard (group III) patients with chronic hepatitis B virus there was negative significant correlation between serum IL-10 and IL-1B (r=-0.63, P<0.05), but no significant correlation between serum IL-10 and serum IL-6 and there was highly positive correlation between serum IL-1B and serum IL-6 (r=0.90, P<0.01). Ten patients with chronic hepatitis C&B virus (group VI) showed highly negative significant correlation between serum IL-10 and each of serum IL-1B and serum IL-6 (r=-0.82, P<0.01) (r=-0.80, P<0.01) respectively. There was highly significant positive correlation between serum IL-1B and serum IL-6 (r=0.88, P<0.01) and significant correlation between serum IL-1B and serum ALT(r=0.63, P<0.05), and prothrombin concentration (r=0.67, P<0.05). A significant correlation between the level of serum IL-1B, IL-6, and serum IL-10 and degree of fibrosis was found. The increase in serum level of IL-1B, IL-6 was associated with increase the degree of fibrosis but the mild and moderate fibrosis were associated with higher level of IL-10 while patients with marked degree of fibrosis were associated with lower level of IL-10.