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iral hepatic disease can progress into more serious pathological outcomes and eventually to hepatocellular carcinoma .The pathogenesis of liver cell injury in chronic hepatitis C infection is poorly understood. Previous studies have demonstrated that T-cell immunoregulatory cytokines contribute to liver damage.
Activation of the cellular immune response is implicated in the eradication of HCV infection, The Th1 profile appears to be associated with the benign and favorable clinical outcome in HCV infection. A prevalent Th2 response may contribute to the chronicity of HCV infection and the severity of liver disease.
Human interleukin-17 (IL-17)-producing CD4Tcells, Th17, comprise a proinflammatory T-cell subset. Several key cytokines, including IL-1, IL-6, tumor necrosis factor alpha, and IL-23 create a cytokinemilieu that regulates the differentiation and expansion of human Th17 cell IL-17A can mobilize, recruit, and activate neutrophils, leading to massive tissue inflammation, and promote the progression of autoimmune disease. Furthermore, serum IL-17 levels are increased and serve as a marker of the severity of acute hepatic injury.
Zinc one of the essential trace elements, is required by many enzymes and transcription factors for their activity or the maintenance of their structure. It has a variety of effects in the immune system. Zn deficiency causes an imbalance between Th1and Th2 function in periphery. Production of IFN-gamma and IL-2, Th1 products, are decreased, whereas productions of IL-4, IL-6 andIL-10, Th2 products, are not affected.
The main zinc metabolism occurs in the liver hepatocytes. It has been demonstrated that Zn may play an important role as a negative regulator of HCV replication in genome length RNA-replicating cells.
Zinc uses claimed to suppress Th17-mediated autoimmune diseases at least in part by inhibiting the development of Th17 cells via attenuating STAT3 activation.
The present study was undertaken aiming to evaluate the plasma concentration of Zinc and IL-17 in patients with chronic hepatitis C liver disease, and also to asses if there is a relation Zn and IL-17.
Two groups of individuals were included in the study patients group, including 16denevo chronic HCV patients, 17compensated chronic HCV patients and 17 decompensated chronic HCV patients, control group that included 30 age and sex matched normal healthy controls. Quantitative assays of serum IL-17 and Zn, using commercially supplied ELISA and spectrophotometer were performed for all individuals.
Statistically high significant differences as regards serum levels of IL-17 and Zn were found between the studied groups; patients group had higher levels of IL-17 and lower levels of Zn. Additionally, correlation studies have revealed significant positive correlations between IL-17 and each of serum albumin, P.T., and INR.
And a significant positive correlations between Zn and each of serum albumin, P.T., and INR and a significant negative correlation between IL-17and Zn.
In conclusion: we have shown that high levels of IL-17 are associated with the severity of liver injury and it could be used as a predictor to the degree of liver damage. Also we have shown that Zn deficiency increases with the severity of the disease. So still more studies are required to test whether Zn deficiency is the cause of high levels of IL-17 or not also more studies are needed to clarify whether Zn supplementation to the patients of early chronic HCV will be helpful to prevent further damage or not.