Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection

Hepatitis C virus (HCV)-induced liver disease contributes to chronic hepatitis. The immune factors identified in HCV include changes in the innate and adaptive immune system. The inflammatory mediators, known as “inflammasome”, are a consequence of the metabolic products of cells and commensal or pa...

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Main Authors: Manuela G. Neuman, Lawrence B. Cohen
Format: Article
Language:English
Published: MDPI AG 2021-11-01
Series:Current Issues in Molecular Biology
Subjects:
Online Access:https://www.mdpi.com/1467-3045/43/3/139
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author Manuela G. Neuman
Lawrence B. Cohen
author_facet Manuela G. Neuman
Lawrence B. Cohen
author_sort Manuela G. Neuman
collection DOAJ
description Hepatitis C virus (HCV)-induced liver disease contributes to chronic hepatitis. The immune factors identified in HCV include changes in the innate and adaptive immune system. The inflammatory mediators, known as “inflammasome”, are a consequence of the metabolic products of cells and commensal or pathogenic bacteria and viruses. The only effective strategy to prevent disease progression is eradication of the viral infection. Immune cells play a pivotal role during liver inflammation, triggering fibrogenesis. The present paper discusses the potential role of markers in cell death and the inflammatory cascade leading to the severity of liver damage. We aim to present the clinical parameters and laboratory data in a cohort of 88 HCV-infected non-cirrhotic and 25 HCV cirrhotic patients, to determine the characteristic light microscopic (LM) and transmission electron microscopic (TEM) changes in their liver biopsies and to present the link between the severity of liver damage and the serum levels of cytokines and caspases. A matched HCV non-infected cohort was used for the comparison of serum inflammatory markers. We compared the inflammation in HCV individuals with a control group of 280 healthy individuals. We correlated the changes in inflammatory markers in different stages of the disease and the histology. We concluded that the serum levels of cytokine, chemokine, and cleaved caspase markers reveal the inflammatory status in HCV. Based upon the information provided by the changes in biomarkers the clinician can monitor the severity of HCV-induced liver damage. New oral well-tolerated treatment regimens for chronic hepatitis C patients can achieve cure rates of over 90%. Therefore, using the noninvasive biomarkers to monitor the evolution of the liver damage is an effective personalized medicine procedure to establish the severity of liver injury and its repair.
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spelling doaj.art-e080d379486a4e88b03be693be8b80812023-11-23T07:44:13ZengMDPI AGCurrent Issues in Molecular Biology1467-30371467-30452021-11-014332022203510.3390/cimb43030139Inflammation and Liver Cell Death in Patients with Hepatitis C Viral InfectionManuela G. Neuman0Lawrence B. Cohen1In Vitro Drug Safety and Biotechnology, The Department of Pharmacology and Toxicology, Temerity Faculty of Medicine, University of Toronto, Banting Institute, 100 College St., Toronto, ON M5G 1L5, CanadaSunnybrook Health Sciences Centre, Division of Gastroenterology, Department of Medicine, Temerity Faculty of Medicine, 2075 Bayview Ave., Toronto, ON M4N 3M5, CanadaHepatitis C virus (HCV)-induced liver disease contributes to chronic hepatitis. The immune factors identified in HCV include changes in the innate and adaptive immune system. The inflammatory mediators, known as “inflammasome”, are a consequence of the metabolic products of cells and commensal or pathogenic bacteria and viruses. The only effective strategy to prevent disease progression is eradication of the viral infection. Immune cells play a pivotal role during liver inflammation, triggering fibrogenesis. The present paper discusses the potential role of markers in cell death and the inflammatory cascade leading to the severity of liver damage. We aim to present the clinical parameters and laboratory data in a cohort of 88 HCV-infected non-cirrhotic and 25 HCV cirrhotic patients, to determine the characteristic light microscopic (LM) and transmission electron microscopic (TEM) changes in their liver biopsies and to present the link between the severity of liver damage and the serum levels of cytokines and caspases. A matched HCV non-infected cohort was used for the comparison of serum inflammatory markers. We compared the inflammation in HCV individuals with a control group of 280 healthy individuals. We correlated the changes in inflammatory markers in different stages of the disease and the histology. We concluded that the serum levels of cytokine, chemokine, and cleaved caspase markers reveal the inflammatory status in HCV. Based upon the information provided by the changes in biomarkers the clinician can monitor the severity of HCV-induced liver damage. New oral well-tolerated treatment regimens for chronic hepatitis C patients can achieve cure rates of over 90%. Therefore, using the noninvasive biomarkers to monitor the evolution of the liver damage is an effective personalized medicine procedure to establish the severity of liver injury and its repair.https://www.mdpi.com/1467-3045/43/3/139tumor necrosis factor alphaapoptosomeinflammasomecytokineschemokinesfibrosis
spellingShingle Manuela G. Neuman
Lawrence B. Cohen
Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection
Current Issues in Molecular Biology
tumor necrosis factor alpha
apoptosome
inflammasome
cytokines
chemokines
fibrosis
title Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection
title_full Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection
title_fullStr Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection
title_full_unstemmed Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection
title_short Inflammation and Liver Cell Death in Patients with Hepatitis C Viral Infection
title_sort inflammation and liver cell death in patients with hepatitis c viral infection
topic tumor necrosis factor alpha
apoptosome
inflammasome
cytokines
chemokines
fibrosis
url https://www.mdpi.com/1467-3045/43/3/139
work_keys_str_mv AT manuelagneuman inflammationandlivercelldeathinpatientswithhepatitiscviralinfection
AT lawrencebcohen inflammationandlivercelldeathinpatientswithhepatitiscviralinfection