ArticleJournal of virology2013
Hepatitis C virus infection induces inflammatory cytokines and chemokines mediated by the cross talk between hepatocytes and stellate cells.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Malnutrition, Frailty, and Sarcopenia in Patients With Cirrhosis: 2021 Practice Guidance by the American Association for the Study of Liver Diseases.Hepatology (Baltimore, Md.) · 2021Guideline
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Targeting inflammatory pathways in hepatocellular carcinoma: recent developments.Discover oncology · 2025Review
- Liver Fibrosis Stages Affect Organic Cation Transporter 1/2 Activities in Hepatitis C Virus-Infected Patients.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Studies on the Role of Compartmentalized Profiles of Cytokines in the Risk of Hepatocellular Carcinoma.International journal of molecular sciences · 2023Article
- Nitrate Reductase NarGHJI Modulates Virulence via Regulation ofMicrobiology spectrum · 2023Article
- Innate immunity and early liver inflammation.Frontiers in immunology · 2023Review
- Review
- Significance of elevated serum and hepatic NOD-like receptor pyrin domain containing 3 (NLRP3) in hepatitis C virus-related liver disease.Scientific reports · 2022Article
- The Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Oral Cavity and Abdominal Organs.International journal of molecular sciences · 2022Review
- C-reactive protein to lymphocyte count ratio is a promising novel marker in hepatitis C infection: the clear hep-c study.Revista da Associacao Medica Brasileira (1992) · 2022Article
- Deubiquitination and Activation of the NLRP3 Inflammasome by UCHL5 in HCV-Infected Cells.Microbiology spectrum · 2021Article
- Review
- Emerging Importance of Chemokine Receptor CXCR4 and Its Ligand in Liver Disease.Frontiers in cell and developmental biology · 2021Review
- Excess Weight Gain After Cure of Hepatitis C Infection with Direct-Acting Antivirals.Journal of general internal medicine · 2020Article
- Review
- Article
- Fibrogenic Gene Expression in Hepatic Stellate Cells Induced by HCV and HIV Replication in a Three Cell Co-Culture Model System.Scientific reports · 2019Article
- Article
- Hepatitis C: From inflammatory pathogenesis to anti-inflammatory/hepatoprotective therapy.World journal of gastroenterology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory cytokines and chemokines play important roles in inflammation during viral infection. Hepatitis C virus (HCV) is a hepatotropic RNA virus that is closely associated with chronic liver inflammation, fibrosis, and hepatocellular carcinoma. During the progression of HCV-related diseases, hepatic stellate cells (HSCs) contribute to the inflammatory response triggered by HCV infection. However, the underlying molecular mechanisms that mediate HSC-induced chronic inflammation during HCV infection are not fully understood. By coculturing HSCs with HCV-infected hepatocytes in vitro, we found that HSCs stimulated HCV-infected hepatocytes, leading to the expression of proinflammatory cytokines and chemokines such as interleukin-6 (IL-6), IL-8, macrophage inflammatory protein 1α (MIP-1α), and MIP-1β. Moreover, we found that this effect was mediated by IL-1α, which was secreted by HSCs. HCV infection enhanced production of CCAAT/enhancer binding protein (C/EBP) β mRNA, and HSC-dependent IL-1α production contributed to the stimulation of C/EBPβ target cytokines and chemokines in HCV-infected hepatocytes. Consistent with this result, knockdown of mRNA for C/EBPβ in HCV-infected hepatocytes resulted in decreased production of cytokines and chemokines after the addition of HSC conditioned medium. Induction of cytokines and chemokines in hepatocytes by the HSC conditioned medium required a yet to be identified postentry event during productive HCV infection. The cross talk between HSCs and HCV-infected hepatocytes is a key feature of inflammation-mediated, HCV-related diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.