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Induction of autophagy is associated with acute hepatitis caused by Concanavalin A in mice
Author(s) -
Chang ChihPeng,
Lei HuanYao
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1065.6
Subject(s) - autophagy , concanavalin a , nod , immune system , hepatitis , immunology , chemistry , biology , apoptosis , in vitro , biochemistry , gene
Concanavalin A (Con A) is known to induce acute hepatitis that is mediated by activation of NKT and T‐cell and cytokines production in immunocompetent mice. The observation of Con A‐induced autophagic cell death in hepatocytes via a BNIP3‐mediated autophagic pathway made us re‐evaluate the effect of Con A on mice. In this study, we report that Con A can induce acute hepatitis in SCID or SCID/NOD mice, with kinetics similar to that of BALB/c, but requiring a higher dose of Con A. No lymphocyte infiltrations were found in liver of SCID or SCID/NOD mice, and the cytokine productions were different. An autophagy with LC3‐II conversion was demonstrated in the liver post Con A injection with a quicker kinetics in the BALB/c than SCID mice. Con A induces IFN‐£^ production at early time on BALB/c mice, and enhances LC3‐II conversion in hepatocytes with addition of IFN‐£^ in vitro. Due to the mannose/glucose‐specific binding on cell membrane, Con A can exhibit both autophagic cytotoxicity and immunomodulation on T cells. This dual‐property can cause acute hepatitis that is enhanced by the immune status of the host. In conclusion, Con A can induce autophagy formation in both T cell‐dependent or ‐independent acute hepatitis.