Cytokines and serum amyloid A in the pathogenesis of hepatitis C virus infection |
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| Affiliation: | 1. Laboratory of Molecular Immunology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, University of Leuven, Leuven, 3000, Belgium;2. University of Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019, UMR 8204, Centre d''Infection et d''Immunité de Lille, Lille, France;1. Department of Gastroenterology and Metabolism, Applied Life Sciences, Institute of Biomedical & Health Sciences, Hiroshima University, Hiroshima, Japan;2. Liver Research Project Center, Hiroshima University, Hiroshima, Japan;3. Laboratory for Digestive Diseases, Center for Genomic Medicine, RIKEN, Hiroshima, Japan;4. Natural Science Center for Basic Research and Development, Hiroshima University, Hiroshima, Japan;1. Programa de Pós-Graduação em Imunologia, Universidade Federal da Bahia, Brazil;2. Hospital Universitário Prof. Edgard Santos, Universidade Federal da Bahia, Brazil;3. Faculdade de Farmácia, Laboratório de Pesquisa em Imunologia, Universidade Federal da Bahia, Brazil;1. Department of Immunology and Histocompatibility, University of Thessaly, School of Health Sciences, Faculty of Medicine, Biopolis 41110, Larissa, Greece;2. Molecular Virology Laboratory, Hellenic Pasteur Institute, 11521 Athens, Greece;3. Molecular Biology and Immunobiotechnology Laboratory, Hellenic Pasteur Institute, 11521 Athens, Greece;4. First Department of Internal Medicine, AHEPA Hospital, Aristotle University of Thessaloniki, School of Medicine, 54636 Thessaloniki, Greece;5. Department of Pathology, AHEPA Hospital, Aristotle University of Thessaloniki, School of Medicine, Kyriakidi Str. 1, 546 36 Thessaloniki, Greece;6. Third Department of Internal Medicine, Papageorgiou Hospital, Aristotle University of Thessaloniki, 546 09 Thessaloniki, Greece;1. Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, Tokyo, 113-8655, Japan;2. Project for Cancer Epigenomics, The Cancer Institute of the Japanese Foundation for Cancer Research, Tokyo, 135-8550, Japan |
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| Abstract: | Expression of the acute phase protein serum amyloid A (SAA) is dependent on the release of the pro-inflammatory cytokines IL-1, IL-6 and TNF-α during infection and inflammation. Hepatitis C virus (HCV) upregulates SAA-inducing cytokines. In line with this, a segment of chronically infected individuals display increased circulating levels of SAA. SAA has even been proposed to be a potential biomarker to evaluate treatment efficiency and the course of disease. SAA possesses antiviral activity against HCV via direct interaction with the viral particle, but might also divert infectivity through its function as an apolipoprotein. On the other hand, SAA shares inflammatory and angiogenic activity with chemotactic cytokines by activating the G protein-coupled receptor, formyl peptide receptor 2. These latter properties might promote chronic inflammation and hepatic injury. Indeed, up to 80 % of infected individuals develop chronic disease because they cannot completely clear the infection, due to diversion of the immune response. In this review, we summarize the interconnection between SAA and cytokines in the context of HCV infection and highlight the dual role SAA could play in this disease. Nevertheless, more research is needed to establish whether the balance between those opposing activities can be tilted in favor of the host defense. |
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| Keywords: | Cytokines Serum amyloid A Hepatitis C virus IL-1 IL-6 TNF-α |
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