Spleen-derived lipocalin-2 in the portal vein regulates Kupffer cells activation and attenuates the development of liver fibrosis in mice

Laboratory Investigation; a Journal of Technical Methods and Pathology
Tomonori AoyamaSumio Watanabe

Abstract

The liver has an immune tolerance against gut-derived products from the portal vein (PV). A disruption of the gut-liver axis leads to liver injury and fibrosis. The spleen is connected to the PV and regulates immune functions. However, possible splenic effects on liver fibrosis development are unclear. Lipocalin-2 (Lcn2) is an antimicrobial protein that regulates macrophage activation. To clarify the role of the spleen in liver fibrosis development, we induced liver fibrosis in mice after splenectomy, and investigated liver fibrosis development. Liver fibrosis resulted in significantly increased splenic Lcn2 levels, but all other measured cytokine levels were unchanged. Splenectomized mice showed enhanced liver fibrosis and inflammation accompanied by significantly decreased Lcn2 levels in PV. Lipopolysaccharide-stimulated primary Kupffer cells, resident liver macrophages, which were treated with recombinant Lcn2 (rLcn2) produced less tumor necrosis factor-α and Ccl2 and the activation of hepatic stellate cells, the effector cells for collagen production in the liver, was suppressed by co-culture with rLcn2-treated Kupffer cells. In addition, the involvement of gut-derived products in splenectomized mice was evaluated by gut st...Continue Reading

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Citations

Dec 19, 2019·Frontiers in Immunology·Daphne van der HeideRuchi Bansal
Jun 7, 2019·Hepatology Communications·Adrien Guillot, Frank Tacke
Aug 4, 2019·Critical Care : the Official Journal of the Critical Care Forum·Fanglin LuHiroshi Morisaki
May 1, 2021·Biomedicines·Melanie A KimmMoritz Wildgruber
May 10, 2021·Liver International : Official Journal of the International Association for the Study of the Liver·Da ChengXin Ni

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