Chronic mineral-oil intraperitoneal administration induces hepatic inflammation through innate immune responses via myeloid cell activation. Lcn2 null mice develop less inflammation due to defective genes involved in myeloid cell activation, and downregulated gene sets for collagen-containing extracellular matrix, leading to mitigation of the liver fibrosis. Lcn2 null mice show enriched expression of genes responsible for DNA damage and cell cycle DNA replication compared to wild-type upon chronic CCl4 liver injury.
- Erawan Borkham-Kamphorst
- Ute Haas
- Ralf Weiskirchen
