Differential interferon signaling in liver lobule and portal area cells under treatment for chronic hepatitis C
Open accessAbstract
Background & aims The mechanisms of treatment resistance to interferon (IFN) and ribavirin (Rib) combination therapy for hepatitis C virus (HCV) infection are not known. This study aims to gain insight into these mechanisms by exploring hepatic gene expression before and during treatment.Methods Liver biopsy was performed in 50 patients before therapy and repeated in 30 of them 1week after initiating combination therapy. The cells in liver lobules (CLL) and the cells in portal areas (CPA) were obtained from 12 patients using laser capture microdissection (LCM).Results Forty-three patients were infected with genotype 1 HCV, 20 of who were viral responders (genotype 1-Rsp) with treatment outcome of SVR or TR, while 23 were non-responders (genotype 1-nonRsp) with NR. Only seven patients were infected with genotype 2. Before treatment, the expression of IFN and Rib-stimulated genes (IRSGs), apoptosis-associated genes, and immune reaction gene pathways was greater in genotype 1-nonRsp than in Rsp. During treatment, IRSGs were induced in genotype 1-Rsp, but not in nonRsp. IRSG induction was irrelevant in genotype 2-Rsp and was mainly impaired in CLL but not in CPA. Pathway analysis revealed that many immune regulatory pathways were induced in CLL from genotype 1-Rsp, while growth factors related to angiogenesis and fibrogenesis were more induced in CPA from genotype 1-nonRsp.Conclusions Impaired IRSGs induction in CLL reduces the sensitivity to treatment for genotype 1 HCV infection. CLL and CPA in the liver might be differentially involved in treatment resistance. These findings could be useful for the improvement of therapy for HCV infection.
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A striking (>60-fold) and robust induction of NCOA7-B occurs in peripheral blood mononuclear cells and macrophages treated with interferon-β-1b (IFNβ1b) or LPS.
“A striking (>60-fold) and robust induction of NCOA7-B occurs in peripheral blood mononuclear cells and macrophages treated with interferon-β-1b (IFNβ1b) or LPS.”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [189]
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- Authors
- Honda, M., Nakamura, M., Tateno, M., Sakai, A., Shimakami, T., Shirasaki, T., Yamashita, T., Arai, K., Yamashita, T., Sakai, Y., & Kaneko, S.
- Affiliations
- Kanazawa University (JP)
- Corresponding author
- Kaneko, Shuichi
- ORCID
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2010-11
- Volume
- 53
- Issue
- 5
- Pages
- 817-826
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W2048807529
- Cited by
- 21
- References
- 21
- Citations by year
- 2023: 1 · 2022: 2 · 2020: 1 · 2019: 2 · 2017: 3 · 2014: 6 · 2013: 2 · 2012: 1
- FWCI
- 1.25
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- cc-by-nc-nd
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- Locations
- Journal of Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Kanazawa University Repository for Academic Resources (DSpace) (Kanazawa University) (submittedVersion, cc-by-nc-nd)
- Funders
- Japan Society for the Promotion of Science (21390227)
- Topics
- Health Sciences › Medicine › Hepatology › Hepatitis C virus research
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- chronic hepatitis C, interferon signaling, ribavirin, treatment resistance, liver lobule, portal area, HCV genotype 1, HCV genotype 2, hepatic gene expression, apoptosis, angiogenesis, liver fibrogenesis, viral response
- MeSH terms
- Interferon alpha-2, Adult, Aged, Drug Therapy, Combination, Female, Humans, Immunity, Innate, Liver, Male, Middle Aged, Recombinant Proteins, Ribavirin, RNA, Viral, Signal Transduction, Interferon-alpha, Hepatitis C, Chronic, Gene Expression Profiling
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