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Galectin-3 deficien...
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Volarevic, Vladislav
(författare)
Galectin-3 deficiency prevents concanavalin A-induced hepatitis in mice
- Artikel/kapitelEngelska2012
Förlag, utgivningsår, omfång ...
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2012-04-25
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Ovid Technologies (Wolters Kluwer Health),2012
Nummerbeteckningar
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LIBRIS-ID:oai:lup.lub.lu.se:b5da7c3c-ffb1-4b07-8e43-0c1b1fc2f0e0
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https://lup.lub.lu.se/record/2906506URI
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https://doi.org/10.1002/hep.25542DOI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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Ämneskategori:ref swepub-contenttype
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We used concanavalin A (Con A)-induced liver injury to study the role of galectin-3 (Gal-3) in the induction of inflammatory pathology and hepatocellular damage. We tested susceptibility to Con Ainduced hepatitis in galectin-3-deficient (Gal-3-/-) mice and analyzed the effects of pretreatment with a selective inhibitor of Gal-3 (TD139) in wild-type (WT) C57BL/6 mice, as evaluated by a liver enzyme test, quantitative histology, mononuclear cell (MNC) infiltration, cytokine production, intracellular staining of immune cells, and percentage of apoptotic MNCs in the liver. Gal-3-/- mice were less sensitive to Con Ainduced hepatitis and had a significantly lower number of activated lymphoid and dendritic cells (DCs) in the liver. The level of tumor necrosis factor alpha (TNFa), interferon gamma (IFN?), and interleukin (IL)-17 and -4 in the sera and the number of TNFa-, IFN?-, and IL-17- and -4-producing cluster of differentiation (CD)4+ cells as well as IL-12-producing CD11c+ DCs were lower, whereas the number of IL-10-producing CD4+ T cells and F4/80+ macrophages were significantly higher in livers of Gal-3-/- mice. Significantly higher percentages of late apoptotic Annexin V+ propidium-idodide+ liver-infiltrating MNCs and splenocytes were observed in Gal-3-/- mice, compared to WT mice. Pretreatment of WT C57BL/6 mice with TD139 led to the attenuation of liver injury and milder infiltration of IFN?- and IL-17- and -4-producing CD4+ T cells, as well as an increase in the total number of IL-10-producing CD4+ T cells and F4/80+ CD206+ alternatively activated macrophages and prevented the apoptosis of liver-infiltrating MNCs. Conclusions: Gal-3 plays an important proinflammatory role in Con Ainduced hepatitis by promoting the activation of T lymphocytes and natural killer T cells, maturation of DCs, secretion of proinflammatory cytokines, down-regulation of M2 macrophage polarization, and apoptosis of MNCs in the liver. (HEPATOLOGY 2012;55:19541964)
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Milovanovic, Marija
(författare)
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Ljujic, Biljana
(författare)
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Pejnovic, Nada
(författare)
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Arsenijevic, Nebojsa
(författare)
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Nilsson, UlfLund University,Lunds universitet,Centrum för analys och syntes,Kemiska institutionen,Institutioner vid LTH,Lunds Tekniska Högskola,Centre for Analysis and Synthesis,Department of Chemistry,Departments at LTH,Faculty of Engineering, LTH(Swepub:lu)ok2-uni
(författare)
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Leffler, Hakon
(författare)
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Lukic, Miodrag L.
(författare)
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Centrum för analys och syntesKemiska institutionen
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Hepatology: Ovid Technologies (Wolters Kluwer Health)55:6, s. 1954-19641527-33500270-9139
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