Those who prefer unhealthier food have higher prevalence of GI symptoms. Conclusions: These data suggest that psycho-behavioral conditions may affect the development of functional GI symptoms regardless of the subtypes of GI symptoms, and may explain the high proportion of overlap in the subtypes. “
“The necroinflammatory reaction plays a central role in hepatitis B virus (HBV) elimination. Cluster of differentiation (CD)8-positive cytotoxic T lymphocytes (CTLs) are thought to be a main player in the elimination of infected cells, and a recent report suggests that natural
killer (NK) Stem Cells inhibitor cells also play an important role. Here, we demonstrate the elimination of HBV-infected hepatocytes by NK cells and dendritic cells (DCs) using urokinase-type plasminogen activator/severe combined immunodeficiency mice, in which the livers were highly repopulated with human hepatocytes. After establishing HBV infection, we injected human peripheral blood mononuclear cells (PBMCs) into the mice and analyzed liver pathology and infiltrating human immune cells with flow cytometry. Severe hepatocyte degeneration was observed only in HBV-infected mice transplanted with human PBMCs. We provide the first direct evidence that massive
liver cell death can be caused by Fas/Fas ligand (FasL) interaction provided by NK cells activated by DCs. Treatment of mice with anti-Fas antibody completely prevented severe hepatocyte degeneration. Furthermore, severe hepatocyte death can be prevented by CDK inhibitor depletion of DCs, whereas depletion of CD8-positive CTLs did not disturb the development
of massive liver cell apoptosis. Conclusion: Our findings provide the first direct evidence that DC-activated NK cells induce Epothilone B (EPO906, Patupilone) massive HBV-infected hepatocyte degeneration through the Fas/FasL system and may indicate new therapeutic implications for acute severe/fulminant hepatitis B. (HEPATOLOGY 2012) Between 4% and 32% of fulminant hepatitis cases, characterized by acute massive hepatocyte degeneration and subsequent development of hepatic encephalopathy and liver failure, are caused by acute hepatitis B virus (HBV) infection.1 Host2 and viral factors3 may influence the development of fulminant hepatitis, but these factors have not been fully elucidated. Innate and adaptive immunity both play a role in the elimination of viral infections. In the innate immune response, cytoplasmic and membrane-bound receptors recognize viruses and induce interferon (IFN)-β production, which, in turn, up-regulates IFN-α and induces an antiviral state in surrounding cells.4 In the adaptive immune response, viruses are recognized by dendritic cells (DCs), which activate cluster of differentiation (CD)8-positive T cells to reduce viral replication through cytolytic5 and noncytolytic mechanisms.