Browsing by Author "Milovanovic, Jelena (54881059800)"
Now showing 1 - 3 of 3
- Results Per Page
- Sort Options
- Some of the metrics are blocked by yourconsent settings
Publication Gal-3 deficiency suppresses novosphyngobium aromaticivoransinflammasome activation and IL-17 driven autoimmune cholangitis in mice(2019) ;Arsenijevic, Aleksandar (56256062100) ;Milovanovic, Jelena (54881059800) ;Stojanovic, Bojana (56460994800) ;Djordjevic, Dragana (57192591516) ;Stanojevic, Ivan (55798544900) ;Jankovic, Nenad (55747362600) ;Vojvodic, Danilo (6603787420) ;Arsenijevic, Nebojsa (6507926547) ;Lukic, Miodrag L. (7005792112)Milovanovic, Marija (35746581300)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. © 2019 Arsenijevic, Milovanovic, Stojanovic, Djordjevic, Stanojevic, Jankovic, Vojvodic, Arsenijevic, Lukic and Milovanovic. - Some of the metrics are blocked by yourconsent settings
Publication Gal-3 deficiency suppresses novosphyngobium aromaticivoransinflammasome activation and IL-17 driven autoimmune cholangitis in mice(2019) ;Arsenijevic, Aleksandar (56256062100) ;Milovanovic, Jelena (54881059800) ;Stojanovic, Bojana (56460994800) ;Djordjevic, Dragana (57192591516) ;Stanojevic, Ivan (55798544900) ;Jankovic, Nenad (55747362600) ;Vojvodic, Danilo (6603787420) ;Arsenijevic, Nebojsa (6507926547) ;Lukic, Miodrag L. (7005792112)Milovanovic, Marija (35746581300)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. © 2019 Arsenijevic, Milovanovic, Stojanovic, Djordjevic, Stanojevic, Jankovic, Vojvodic, Arsenijevic, Lukic and Milovanovic. - Some of the metrics are blocked by yourconsent settings
Publication Predictive parameters of mortality in patients with metabolic syndrome undergoing hemodialysis(2019) ;Stolic, Radojica V. (9739642000) ;Trajkovic, Goran Z. (9739203200) ;Pavlovic, Vedrana (57202093978) ;Pajovic, Slavica (56066439900) ;Lazic, Snezana (57140141800) ;Milinic, Srbislava (55979728100) ;Milovanovic, Jelena (54881059800) ;Matejic, Slavisa (57213391810) ;Jaksic, Masa (57196713448)Matijasevic, Ivana (59874458100)Introduction: Metabolic syndrome is considered as one at the most important public health problems and in hemodialysis patients it is one of the main factors of mortality. The aim of the study was to determine the predictive parameters of the mortality of patients with metabolic syndrome. Materials and methods: In a nine-year study, the outcome of the clinical treatment of 108 hemodialysis patients was analyzed, divided into a group of patients with metabolic syndrome and group of patients without metabolic syndrome. The demographic, anthropometric, clinical and laboratory characteristics of the examinees were evaluated. Results: Mortality of patients with metabolic syndrome was 28.1% and in the group of patients without metabolic syndrome 13.2%. Statistically significant difference was found between the group of patients with and without metabolic syndrome in comparison with body mass index (p <0.001), age (p = 0.027), diabetic nephropathy (p <0.001), number of comorbidities (p <0.001), the number of leukocytes (p = 0.043), total proteins (p = 0.044), albumin (p = 0.001), calcium (p = 0.016), glycemia (p = 0.002) and creatinine (p = 0.032). Predictive parameters of survival in patients on hemodialysis with metabolic syndrome are the body mass index (B - 0.056; SE 0.008; p <0.001) and diabetic nephropathy (B 0.397; SE 0.098; p <0.001). Conclusion: Lower body mass index and diabetic nephropathy are, in our study, the predictive parameters of mortality of patients on hemodialysis. © 2019 A. CARBONE Editore. All rights reserved.
