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Gal-3 has the role in multiple inflammatory pathways. Multiple-hit etiology of primary biliary cholangitis (PBC) and evolving immune response at various stages of the disease includes involvement of Gal-3 in PBC pathogenesis. In this study we aimed to clarify the role of Gal-3 in  Novosphingobium aromaticivorans  ( N. aromaticivorans ) induced biliary disease. Autoimmune cholangitis was induced in mice by two intra-peritoneal injections of  N. aromaticivorans  within 2 weeks. The role of Gal-3 was evaluated by using Lgals3 −/−  mice and mice treated with Gal-3 inhibitor. The histological and serological parameters of disease, phenotype of dendritic, NK, NKT, and T cells and inflammasome expression were evaluated. Marked attenuation of the disease in Lgals3 −/−  and Gal-3 inhibitor, DAVANAT ® , treated mice is manifested by the absence of bile duct damage, granulomas and fibrosis. Liver infiltrates of  N. aromaticivorans  infected wild type mice had higher incidence of pro-inflammatory macrophages, dendritic cells, NK, NKT, and T cells. Lgals3 deletion and treatment with Gal-3 inhibitor reduced inflammatory mononuclear cell infiltrate, expression of NLRP3 inflammasome in the liver infiltrates and interleukin-1β (IL-1β) production in the livers of  N. aromaticivorans  infected mice.  In vitro  stimulation of wild type peritoneal macrophages with  N. aromaticivorans  caused increased NLRP3 expression, caspase-1 activity and IL-1β production compared with Lgals3 −/−  cells. Our data highlight the importance of Gal-3 in promotion of inflammation in  N. aromaticivorans  induced PBC by enhancing the activation of NLRP3 inflammasome and production of IL-1β and indicate Gal-3 as possible therapeutical target in autoimmune cholangitis. Galectin-3 appears involved in inflammatory response to gut commensal leading to PBC.

Gal-3 Deficiency Suppresses Novosphyngobium aromaticivorans Inflammasome Activation and IL-17 Driven Autoimmune Cholangitis in Mice