ArticleHepatology communications2025
Interleukin-18 binding protein protects against metabolic steatohepatitis.
Article in Hepatology communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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18 authors.
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Abstract
backgroundMetabolic dysfunction-associated steatohepatitis (MASH) is a frequent consequence of Western diet consumption and liver steatosis. IL-18 binding protein (IL-18BP) limits the action of interleukin-18 (IL-18). Our work aims to study the unknown role of IL-18BP in MASH progression.
methodsWe analyzed the liver transcriptome from MASH patients. We investigated cell-specific expressions of IL-18, IL-18BP, and IL-18 receptor in human and mouse liver. We studied the liver phenotype of Il18bp-/- mice on a high-fat/high-cholesterol (HFHC) diet. We administered an anti-IL-18 antibody in Il18bp-/- mice and in diet-induced wild-type (WT) MASH mice. We generated and studied double knock-out Il18bp-/-Ifng-/- mice.
resultsIL-18BP expression is increased in the liver of patients and mouse models with MASH and positively correlates with fibrosis stages. On the HFHC diet, Il18bp-/- mice exhibit increased hepatic damage, inflammation, and fibrosis compared with WT mice. Treatment with anti-IL-18 antibody corrects liver defects in Il18bp-/- mice and ameliorates inflammation and fibrosis in diet-induced MASH mice, suggesting a translational treatment opportunity. Genetic deficiency in IFN-γ abrogates inflammation but not fibrosis in Il18bp-/- mice.
conclusionsIL-18BP has a role in limiting the progression of MASH, notably by reducing inflammation and fibrosis. Downstream IL-18 over-signaling, IFN-γ, mediates inflammation, but not fibrosis. Increasing IL-18BP levels represents a novel therapeutic perspective for patients affected by MASH.
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