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Galectin‐1 exerts immunomodulatory and protective effects on concanavalin a–induced hepatitis in mice
Author(s) -
Santucci Luca,
Fiorucci Stefano,
Cammilleri Francesco,
Servillo Giuseppe,
Federici Barbara,
Morelli Antonio
Publication year - 2000
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510310220
Subject(s) - concanavalin a , galectin 3 , hepatitis , galectin 1 , immunology , pharmacology , medicine , cancer research , chemistry , biochemistry , in vitro
Galectin‐1, an endogenous lectin with immunomodulatory activities, induces selective, Fas‐independent apoptosis of activated T cells. The aim of the present study was to evaluate the effect galectin‐1 exerts on concanavalin A (Con A)–induced hepatitis, a T‐cell–dependent model of liver injury. Con A administration resulted in liver injury, as shown by the increased transaminase plasma levels and liver DNA fragmentation, and caused spleen T‐cell activation, which was associated with a strong increment in liver infiltrating T helper cells. Moreover, Con A injection leads to a marked increase in plasma tumor necrosis factor α (TNF‐α) and interferon gamma (IFN‐γ) levels. Galectin‐1 pretreatment dose‐dependently prevented both liver injury and T‐helper cell liver infiltration induced by Con A. In vivo and in vitro experiments indicated that the protective effects of galectin‐1 depend on the selective elimination of Con A–activated T cells. In addition, galectin‐1 almost completely prevented the Con A–induced increase in plasma TNF‐α and IFN‐γ, an effect that was, at least in part, independent on the elimination of activated T helper cells, because galectin‐1 prevented lipopolysaccharide (LPS)‐induced release of TNF‐α and IFN‐γ also from macrophages in vitro , without affecting their viability. The present study suggests that galectin‐1 is potentially useful in the treatment of T‐cell–mediated human liver disorders.