HCV-induced regulatory alterations of IL-1β, IL-6, TNF-α, and IFN-ϒ operative, leading liver en-route to non-alcoholic steatohepatitis

Over the course of time, Hepatitis C has become a universal health menace. Its deleterious effects on human liver encompass a lot of physiological, genetic as well as epigenetic alterations. Fatty liver (Hepatic steatosis) is an inflammation having multifactorial ancestries; one of them is HCV (stea...

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Bibliographic Details
Published in:Inflammation research 2017-06, Vol.66 (6), p.477-486
Main Authors: Nawaz, Rabia, Zahid, Sadia, Idrees, Muhammad, Rafique, Shazia, Shahid, Muhammad, Ahad, Ammara, Amin, Iram, Almas, Iqra, Afzal, Samia
Format: Article
Language:English
Subjects:
Allergology
Animals
Biomedical and Life Sciences
Biomedicine
Cytokines - immunology
Dermatology
Hepacivirus
Hepatitis C - immunology
Humans
Immunology
Liver - immunology
Neurology
Non-alcoholic Fatty Liver Disease - immunology
Pharmacology/Toxicology
Review
Rheumatology
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Summary:Over the course of time, Hepatitis C has become a universal health menace. Its deleterious effects on human liver encompass a lot of physiological, genetic as well as epigenetic alterations. Fatty liver (Hepatic steatosis) is an inflammation having multifactorial ancestries; one of them is HCV (steatohepatitis). HCV boosts several cellular pathways involving up-regulation of a number of cytokines. Current study reviews the regulation of some selective key cytokines during HCV infection, to help generate an improved understanding of their role. These cytokines, IL-1β, IL-6, TNF-α, and IFN-ϒ, are inflammatory markers of the body. These particular markers along with others help hepatocytes against viral infestation. However, recently, their association has been found in degradation of liver on the trail heading to non-alcoholic steatohepatitis (NASH). Consequently, the disturbance in their equilibrium has been repeatedly reported during HCV infection. Quite a number of findings are affirming their up-regulation. Although these cell markers are stimulated by hepatocytes as their standard protection mechanism, but modern studies have testified the paradoxical nature of this defense line. Nevertheless, direct molecular or epigenetic research is needed to question the actual molecular progressions and directions commanding liver to steatosis, cirrhosis, or eventually HCC (Hepatocellular Carcinoma).
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-017-1029-3