AI Article Synopsis
- Inflammation and metabolic dysfunction are key factors in non-alcoholic fatty liver disease (NAFLD), which is rapidly increasing globally.
- Researchers studied 142 NAFLD patients to explore the genetic link between specific IFNL4 variants and fibrosis, finding a higher frequency of a non-functional IFNL4 allele in patients with significant fibrosis.
- Contrary to expectations, experiments in an animal model revealed that interferon treatment led to increased liver fibrosis, highlighting a complex relationship between IFN and fibrosis development.
Article 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.
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| http://dx.doi.org/10.1038/s41435-022-00176-6 | DOI Listing |
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