Hepatitis-related hepatocellular carcinoma: Insights into cytokine gene polymorphisms.

Hepatocellular carcinoma (HCC) is a primary liver cancer, which is one of the most prevalent cancers among humans. Many factors are involved in the liver carcinogenesis as lifestyle and environmental factors. Hepatitis virus infections are now recognized as the chief etiology of HCC; however, the precise mechanism is still enigmatic till now. The inflammation triggered by the cytokine-mediated immune response, was reported to be the closest factor of HCC development. Cytokines are immunoregulatory proteins produced by immune cells, functioning as orchestrators of the immune response. Genes of cytokines and their receptors are known to be polymorphic, which give rise to variations in their genes. These variations have a great impact on the expression levels of the secreted cytokines. Therefore, cytokine gene polymorphisms are involved in the molecular mechanisms of several diseases. This piece of work aims to shed much light on the role of cytokine gene polymorphisms as genetic host factor in hepatitis related HCC.

Impact of Schistosoma mansoni and Echinococcus granulosus experimental coinfection on interleukin 10 and interferon gamma cytokines profile.

The interactions between various aspects of the immune responses mediated by concomitant parasite infections may influence the resultant cytokines profiles. We tested this hypothesis by developing two Schistosoma mansoni and Echinococcus granulosus coinfection murine models. Our aim was to explore the effect of echinoccocis on the immune responses induced by schistosomiasis, either when the two infections were induced synchronously or when echinococcosis was induced during egg deposition period of S. mansoni infection. The proliferation of antigens specific stimulated splenocytes, taken from studied groups, was determined. Then, IFN-γ, and IL-10 production from stimulated cells were measured. Significant elevation of IFN-γ, 4weeks after synchronous coinfection, was occurred compared to S. mansoni infected group, associated with modest elevation of IL10 level. On the other hand, echinococcosis coinfection during egg deposition period of schistosomiasis resulted in significant marked reduction in IL10 level in comparison to S. mansoni infected mice. These results suggested that echinococcosis coinfection, during the switching from Th1 to Th2 cytokine stage of murine schistosomiasis, can alter the ability of S. mansoni infection to skew the cytokines response towards Th2 profile. It is clear that the timing and sequence of concomitant infections are of vital importance for the outcome of the immune response.