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Polymicrobial Sepsis-Induced Changes in Hepatic Stellate Cell Communication in Male C57BL/6J Mice
Steven Timmermans1,2, Céline Van Dender1,2, Maxime Roes1,2
1Center for Inflammation Research, Vlaams Instituut voor Biotechnologie (VIB), 9052 Ghent, Belgium.
Cells
|June 11, 2026
Summary
Sepsis causes liver dysfunction and fibrosis. Hepatic stellate cells (HSCs) become key signaling hubs, suppressing liver cell function and promoting injury during septic acute liver injury.
Area of Science:
- Hepatology
- Immunology
- Systems Biology
Background:
- Sepsis induces severe liver dysfunction, characterized by metabolic changes and maladaptive repair, potentially leading to fibrosis instead of regeneration.
- Intercellular communication plays a critical role in determining sepsis-induced liver outcomes.
Purpose of the Study:
- To investigate how cell-cell communication influences liver outcomes during septic acute liver injury.
- To identify key cellular players and signaling pathways involved in sepsis-induced liver dysfunction and fibrosis.
Main Methods:
- Cell type-specific bulk RNA-sequencing was performed on hepatocytes, hepatic stellate cells, liver sinusoidal endothelial cells, Kupffer cells, and CD45+ leukocytes from mice with polymicrobial sepsis.
- Cell-cell communication analyses were conducted using CellChat and NicheNet.
Main Results:
- Sepsis significantly reorganized the hepatic cellular communication network.
- Hepatic stellate cells (HSCs) emerged as a central signaling hub, broadcasting fibrogenic and chemotactic signals (e.g., Ccl7).
- HSC signaling suppressed hepatocyte metabolic function, promoted leukocyte infiltration, and initiated fibrogenic priming.
Conclusions:
- Hepatic stellate cells (HSCs) act as key regulators in septic acute liver injury.
- Targeting HSC-mediated communication nodes could mitigate fibrosis and promote liver regeneration and function.
