Please use this identifier to cite or link to this item:
Full metadata record
DC FieldValueLanguage
dc.contributor.authorArsenijevic A.-
dc.contributor.authorMilovanovic, Jelena-
dc.contributor.authorStojanovic B.-
dc.contributor.authorDjordjevic, Dragana-
dc.contributor.authorStanojevic, Ivan-
dc.contributor.authorJanković, Nenad-
dc.contributor.authorVojvodic, Danilo-
dc.contributor.authorArsenijevic, Nebojsa-
dc.contributor.authorLukic, Miodrag-
dc.contributor.authorMilovanovic, Marija-
dc.description.abstract© 2019 Arsenijevic, Milovanovic, Stojanovic, Djordjevic, Stanojevic, Jankovic, Vojvodic, Arsenijevic, Lukic and Milovanovic. 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.-
dc.relation.ispartofFrontiers in Immunology-
dc.titleGal-3 deficiency suppresses novosphyngobium aromaticivoransinflammasome activation and IL-17 driven autoimmune cholangitis in mice-
dc.typejournal article-
Appears in Collections:Faculty of Medical Sciences, Kragujevac
Institute for Information Technologies, Kragujevac

Page views(s)




Files in This Item:
File Description SizeFormat 
10.3389-fimmu.2019.01309.pdf4.66 MBAdobe PDFThumbnail

Items in SCIDAR are protected by copyright, with all rights reserved, unless otherwise indicated.