The presence of interferon affects the progression of non-alcoholic fatty liver disease

Michelle Møhlenberg; Peter Lykke  Eriksen; Tea Lund Laursen; Mette Bak Nielsen; Stephen Jacques Hamilton-Dutoit; Henning Grønbæk; Rune Hartmann; Karen Louise Thomsen

doi:10.1038/s41435-022-00176-6

The presence of interferon affects the progression of non-alcoholic fatty liver disease

Michelle Møhlenberg, Peter Lykke Eriksen, Tea Lund Laursen, Mette Bak Nielsen, Stephen Jacques Hamilton-Dutoit, Henning Grønbæk, Rune Hartmann, Karen Louise Thomsen

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

3 Citations (Scopus)

Abstract

Inflammation and metabolic dysfunction are hallmarks of the progression of non-alcoholic fatty liver disease (NAFLD), which is the fastest-growing liver disease worldwide. Emerging evidence indicates that innate immune mechanisms are essential drivers of fibrosis development in chronic inflammatory liver diseases, including NAFLD. In this study, 142 NAFLD patients were genotyped for three IFNL4 single-nucleotide variants in order to investigate the genetic relationship between IFNL4 and fibrosis in NAFLD patients. We observed an overrepresentation of the non-functional IFNL4 allele in patients with significant fibrosis (>F2). Next, we investigated the potential protective role of interferon (IFN) in relation to the development of liver fibrosis in an animal model of non-alcoholic steatohepatitis (NASH). In contradiction to our hypothesis, the results showed an increase in fibrosis in IFN treated animals. Our study clearly indicates that IFN is able to affect the development of liver fibrosis, although our clinical and experimental data are conflicting.

Original language	English
Journal	Genes and Immunity
Volume	23
Issue	5
Pages (from-to)	157–165
Number of pages	9
ISSN	1466-4879
DOIs	https://doi.org/10.1038/s41435-022-00176-6
Publication status	Published - Aug 2022

Keywords

ALPHA
ASSOCIATION
CLEARANCE
DAMAGE
FIBROSIS
IL28B
INFLAMMATION
POLYMORPHISMS
STEATOHEPATITIS
VARIANT
Antiviral Agents
Disease Progression
Non-alcoholic Fatty Liver Disease/genetics
Animals
Interferons/genetics
Liver/metabolism
Fibrosis
Liver Cirrhosis/genetics

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title = "The presence of interferon affects the progression of non-alcoholic fatty liver disease",

abstract = "Inflammation and metabolic dysfunction are hallmarks of the progression of non-alcoholic fatty liver disease (NAFLD), which is the fastest-growing liver disease worldwide. Emerging evidence indicates that innate immune mechanisms are essential drivers of fibrosis development in chronic inflammatory liver diseases, including NAFLD. In this study, 142 NAFLD patients were genotyped for three IFNL4 single-nucleotide variants in order to investigate the genetic relationship between IFNL4 and fibrosis in NAFLD patients. We observed an overrepresentation of the non-functional IFNL4 allele in patients with significant fibrosis (>F2). Next, we investigated the potential protective role of interferon (IFN) in relation to the development of liver fibrosis in an animal model of non-alcoholic steatohepatitis (NASH). In contradiction to our hypothesis, the results showed an increase in fibrosis in IFN treated animals. Our study clearly indicates that IFN is able to affect the development of liver fibrosis, although our clinical and experimental data are conflicting.",

keywords = "ALPHA, ASSOCIATION, CLEARANCE, DAMAGE, FIBROSIS, IL28B, INFLAMMATION, POLYMORPHISMS, STEATOHEPATITIS, VARIANT, Antiviral Agents, Disease Progression, Non-alcoholic Fatty Liver Disease/genetics, Animals, Interferons/genetics, Liver/metabolism, Fibrosis, Liver Cirrhosis/genetics",

author = "Michelle M{\o}hlenberg and Eriksen, {Peter Lykke} and Laursen, {Tea Lund} and Nielsen, {Mette Bak} and Hamilton-Dutoit, {Stephen Jacques} and Henning Gr{\o}nb{\ae}k and Rune Hartmann and Thomsen, {Karen Louise}",

year = "2022",

month = aug,

doi = "10.1038/s41435-022-00176-6",

language = "English",

volume = "23",

pages = "157–165",

journal = "Genes and Immunity",

issn = "1466-4879",

publisher = "Springer Nature",

number = "5",

}

The presence of interferon affects the progression of non-alcoholic fatty liver disease. / Møhlenberg, Michelle ; Eriksen, Peter Lykke ; Laursen, Tea Lund et al.
In: Genes and Immunity, Vol. 23, No. 5, 08.2022, p. 157–165.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review

TY - JOUR

T1 - The presence of interferon affects the progression of non-alcoholic fatty liver disease

AU - Møhlenberg, Michelle

AU - Eriksen, Peter Lykke

AU - Laursen, Tea Lund

AU - Nielsen, Mette Bak

AU - Hamilton-Dutoit, Stephen Jacques

AU - Grønbæk, Henning

AU - Hartmann, Rune

AU - Thomsen, Karen Louise

PY - 2022/8

Y1 - 2022/8

N2 - Inflammation and metabolic dysfunction are hallmarks of the progression of non-alcoholic fatty liver disease (NAFLD), which is the fastest-growing liver disease worldwide. Emerging evidence indicates that innate immune mechanisms are essential drivers of fibrosis development in chronic inflammatory liver diseases, including NAFLD. In this study, 142 NAFLD patients were genotyped for three IFNL4 single-nucleotide variants in order to investigate the genetic relationship between IFNL4 and fibrosis in NAFLD patients. We observed an overrepresentation of the non-functional IFNL4 allele in patients with significant fibrosis (>F2). Next, we investigated the potential protective role of interferon (IFN) in relation to the development of liver fibrosis in an animal model of non-alcoholic steatohepatitis (NASH). In contradiction to our hypothesis, the results showed an increase in fibrosis in IFN treated animals. Our study clearly indicates that IFN is able to affect the development of liver fibrosis, although our clinical and experimental data are conflicting.

AB - Inflammation and metabolic dysfunction are hallmarks of the progression of non-alcoholic fatty liver disease (NAFLD), which is the fastest-growing liver disease worldwide. Emerging evidence indicates that innate immune mechanisms are essential drivers of fibrosis development in chronic inflammatory liver diseases, including NAFLD. In this study, 142 NAFLD patients were genotyped for three IFNL4 single-nucleotide variants in order to investigate the genetic relationship between IFNL4 and fibrosis in NAFLD patients. We observed an overrepresentation of the non-functional IFNL4 allele in patients with significant fibrosis (>F2). Next, we investigated the potential protective role of interferon (IFN) in relation to the development of liver fibrosis in an animal model of non-alcoholic steatohepatitis (NASH). In contradiction to our hypothesis, the results showed an increase in fibrosis in IFN treated animals. Our study clearly indicates that IFN is able to affect the development of liver fibrosis, although our clinical and experimental data are conflicting.

KW - ALPHA

KW - ASSOCIATION

KW - CLEARANCE

KW - DAMAGE

KW - FIBROSIS

KW - IL28B

KW - INFLAMMATION

KW - POLYMORPHISMS

KW - STEATOHEPATITIS

KW - VARIANT

KW - Antiviral Agents

KW - Disease Progression

KW - Non-alcoholic Fatty Liver Disease/genetics

KW - Animals

KW - Interferons/genetics

KW - Liver/metabolism

KW - Fibrosis

KW - Liver Cirrhosis/genetics

U2 - 10.1038/s41435-022-00176-6

DO - 10.1038/s41435-022-00176-6

M3 - Journal article

C2 - 35725929

SN - 1466-4879

VL - 23

SP - 157

EP - 165

JO - Genes and Immunity

JF - Genes and Immunity

IS - 5

ER -

The presence of interferon affects the progression of non-alcoholic fatty liver disease

Abstract

Keywords

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