Mycobiome dysbiosis and genetic predisposition to elevated IL-17A contribute to fibrosis in MASLD

Liver inflammation and fibrosis are key drivers of the transition from bland steatosis to metabolic dysfunction-associated steatohepatitis (MASH). Our findings identify a combinatorial mechanism in which genetic predisposition to enhanced IL-17A signaling, together with gut mycobiome dysbiosis, promotes MASH development and fibrosis progression. This work highlights the importance of host-mycobiome interactions in shaping inflammatory liver disease and supports further investigation into targeted strategies aimed at modulating IL-17A-mediated immune responses in patients with MASLD. Such approaches may offer novel opportunities for risk stratification and therapeutic intervention.

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Publication Details

Journal
JHEP Reports
Published
2025-12-23
DOI
https://doi.org/10.1016/j.jhepr.2025.101721
Primary Topic
Liver Disease Diagnosis and Treatment
Type
article
Field-Weighted Citation Impact
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article

Mycobiome dysbiosis and genetic predisposition to elevated IL-17A contribute to fibrosis in MASLD

Gianni Panagiotou, Heike M. Hermanns, Michaela Herz, Natalie E. Nieuwenhuizen et al.
JHEP Reports
Liver Disease Diagnosis and Treatment
article

Mycobiome dysbiosis and genetic predisposition to elevated IL-17A contribute to fibrosis in MASLD

Gianni Panagiotou, Heike M. Hermanns, Michaela Herz, Natalie E. Nieuwenhuizen, Monika Rau, Sara Leal Siliceo, Oliver Kurzai, Andreas Geier, Nadja Thielemann, Mohammad H. Mirhakkak, Alexander Maximilian Aldejohann, Thomas Dandekar, Nathalie Reus, Isabell S. Behr, Kerstin Hünniger-Ast, Annika Schöninger, Jürgen Löffler, Ronny Martin, Aia Shehata
article en

Abstract

Liver inflammation and fibrosis are key drivers of the transition from bland steatosis to metabolic dysfunction-associated steatohepatitis (MASH). Our findings identify a combinatorial mechanism in which genetic predisposition to enhanced IL-17A signaling, together with gut mycobiome dysbiosis, promotes MASH development and fibrosis progression. This work highlights the importance of host-mycobiome interactions in shaping inflammatory liver disease and supports further investigation into targeted strategies aimed at modulating IL-17A-mediated immune responses in patients with MASLD. Such approaches may offer novel opportunities for risk stratification and therapeutic intervention.

JHEP ReportsVol. 8(3)
University of Würzburg (DE), Universitätsklinikum Würzburg (DE), Leibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) (DE), Friedrich Schiller University Jena (DE), University of Hong Kong (HK)
Good health and well-being
Openalex Percentile: Top 30%
Liver Disease Diagnosis and Treatment
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