%0 Journal Article %T IL-33 signalling in liver immune cells enhances drug-induced liver injury and inflammation %+ mmunopharmacology, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas %+ Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM) %+ Laboratório de Imunobiofotônica, Departamento de Morfologia %A Antunes, Maísa Mota %A Araújo, Alan Moreira %A Diniz, Ariane Barros %A Pereira, Rafaela Vaz Sousa %A Alvarenga, Débora Moreira %A Araújo, Bruna Araújo %A Rocha, Renata Monti %A Lopes, Maria Alice Freitas %A Marchesi, Sarah Cozzer %A Nakagaki, Brenda Naemi %A Marques, Pedro Elias %A Ryffel, Bernhard %A Quesniaux, Valérie %A Guabiraba Brito, Rodrigo %A Filho, José Carlos Alves %A Cara, Denise Carmona %A Rezende, Rafael Machado %A Menezes, Gustavo Batista %Z CNPq; CAPES; FAPEMIG %< avec comité de lecture %@ 1023-3830 %J Inflammation Research %I Springer Verlag %V 67 %N 1 %P 77-88 %8 2018-01 %D 2018 %R 10.1007/s00011-017-1098-3 %M 29032512 %K DAMPs %K ST2 %K Liver necrosis %K leucocyte %K neutrophil %K IL-33 %Z Life Sciences [q-bio] %Z Life Sciences [q-bio]/ImmunologyJournal articles %X The aim of this study was to investigate the contribution of IL-33/ST2 axis in the onset and progression of acute liver injury using a mice model of drug-induced liver injury (DILI). DILI was induced by overdose administration of acetaminophen (APAP) by oral gavage in wild-type BALB/c, ST2-deficient mice and in different bone marrow chimeras. Neutrophils were depleted by anti-Ly6G and macrophages with clodronate liposomes (CLL). Blood and liver were collected for biochemical, immunologic and genetic analyses. Mice were imaged by confocal intravital microscopy and liver non-parenchymal cells and hepatocytes were isolated for flow cytometry, genetic and immunofluorescence studies. Acetaminophen overdose caused a massive necrosis and accumulation of immune cells within the liver, concomitantly with IL-33 and chemokine release. Liver non-parenchymal cells were the major sensors for IL-33, and amongst them, neutrophils were the major players in amplification of the inflammatory response triggered by IL-33/ST2 signalling pathway. Blockage of IL-33/ST2 axis reduces APAP-mediated organ injury by dampening liver chemokine release and activation of resident and infiltrating liver non-parenchymal cells. %G English %L hal-02126492 %U https://cnrs.hal.science/hal-02126492 %~ CNRS %~ UNIV-ORLEANS %~ TEST-HALCNRS