Increased Intrahepatic Mast Cell Density in Liver Cirrhosis Due to MASLD and Other Non-Infectious Chronic Liver Diseases

Nicolás Ortiz-López; Araceli Pinto-León; Javiera Favi; Dannette Guíñez Francois; Larissa Aleman; Laura Carreño-Toro; Alejandra Zazueta; Fabien Magne; Jaime Poniachik; Caroll J. Beltrán

doi:10.3390/ijms27010392

Increased Intrahepatic Mast Cell Density in Liver Cirrhosis Due to MASLD and Other Non-Infectious Chronic Liver Diseases

Journal

International Journal of Molecular Sciences

ISSN

1422-0067

Date Issued

2025-12-30

Author(s)

Nicolás Ortiz-López

Araceli Pinto-León

Javiera Favi

Dannette Guíñez Francois

Larissa Aleman

Laura Carreño-Toro

Alejandra Zazueta

Facultad de Medicina Clínica Alemana Universidad del Desarrollo

Fabien Magne

Jaime Poniachik

Caroll J. Beltrán

Type

journal-article

DOI

10.3390/ijms27010392

URL

https://hdl.handle.net/123456789/12112

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become highly prevalent worldwide, and its pathogenesis and progression mechanisms remain incompletely understood. An increased activation of innate immune cells in the liver contributes to hepatic fibrogenesis via a chronic loop of inflammation and regeneration processes. Among them are mast cells (MCs), whose role in hepatic cirrhosis secondary to MASLD remains poorly studied. Our aim was to evaluate differences in MC density in cirrhotic liver tissue among patients with MASLD and other chronic liver disease etiologies. For this, a retrospective study of MC count was performed in cirrhotic liver explants obtained from MASLD, alcohol-related liver disease (ALD), and autoimmune hepatitis (AIH). We included a control group of subjects without liver damage. Tryptase-positive MCs were identified by indirect immunofluorescence and quantified as MC density per low-power field (MC/LPF). Group differences were analyzed using the Kruskal–Wallis test with Dunn’s multiple comparisons, considering p < 0.05 as statistically significant. A significantly higher MC density was observed in MASLD, ALD, and AIH patients compared with the control group. The group analysis showed that ALD patients exhibited higher MC density than AIH, with no observed difference between ALD and MASLD. MC density was correlated positively with tobacco smoking and alcohol use in the full analyzed group, suggesting them as risk factors of high MC liver infiltration. We conclude that MC density is augmented in MASLD-related cirrhosis, highlighting potential links between lifestyle factors and MC-mediated hepatic inflammation. Future studies should explore the mechanisms driving this association and evaluate whether targeting MCs could help mitigate fibrosis progression.