Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/8407
Title: Galectin-3 deficiency facilitates TNF-α-dependent hepatocyte death and liver inflammation in MCMV infection
Authors: Stojanovic B.
Milovanovic, Jelena
Arsenijevic A.
Stojanovic B.
Geljic I.
Arsenijevic, Nebojsa
Jonjic S.
Lukic, Miodrag
Milovanovic, Marija
Issue Date: 2019
Abstract: © 2007 - 2019 Frontiers Media S.A. All Rights Reserved. Galectin-3 (Gal-3) has a role in multiple inflammatory pathways. Various, opposite roles of Gal-3 in liver diseases have been described but there are no data about the role of Gal-3 in development of hepatitis induced with cytomegalovirus infection. In this study we aimed to clarify the role of Gal-3 in murine cytomegalovirus (MCMV)-induced hepatitis by using Gal-3-deficient (Gal-3 KO) mice. Here we provide the evidence that Gal-3 has the protective role in MCMV-induced hepatitis. Enhanced hepatitis manifested by more inflammatory and necrotic foci and serum level of ALT, enhanced apoptosis and necroptosis of hepatocytes and enhanced viral replication were detected in MCMV-infected Gal-3 deficient mice. NK cells does not contribute to more severe liver damage in MCMV-infected Gal-3 KO mice. Enhanced expression of TNF-α in the hepatocytes of Gal-3 KO mice after MCMV infection, abrogated hepatocyte death, and attenuated inflammation in the livers of Gal-3 KO mice after TNF-α blockade suggest that TNF-a plays the role in enhanced disease in Gal-3 deficient animals. Treatment with recombinant Gal-3 reduces inflammation and especially necrosis of hepatocytes in the livers of MCMV-infected Gal-3 KO mice. Our data highlight the protective role of Gal-3 in MCMV-induced hepatitis by attenuation of TNF-α-mediated death of hepatocytes.
URI: https://scidar.kg.ac.rs/handle/123456789/8407
Type: article
DOI: 10.3389/fmicb.2019.00185
SCOPUS: 2-s2.0-85065910021
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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