Contribution of TIR domain-containing adapter inducing IFN-β-mediated IL-18 release to LPS-induced liver injury in mice

Imamura, Michiko; Tsutsui, Hiroko; Yasuda, Koubun; Uchiyama, Ryosuke; Yumikura‐Futatsugi, Shizue; Mitani, Keiko; Hayashi, Shuhei; Akira, Shizuo; Taniguchi, Shun’ichiro; Rooijen, Nico van; Tschopp, Jürg; Yamamoto, Tetsuya; Fujimoto, Jiro; Nakanishi, Kenji

doi:10.1016/j.jhep.2009.03.027

Cited by 61 publications

(74 citation statements)

References 34 publications

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“…, Caspase-1 2/2 , Asc 2/2 , and Nlrp3 2/2 mice on the B/6 background were maintained in our laboratory (27,28). FasL gld/gld mice on B/6 background were purchased from Japan SLC (Osaka, Japan).…”

Section: /2mentioning

confidence: 99%

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Fas-Mediated Inflammatory Response inListeria monocytogenesInfection

Uchiyama

Yonehara

Tsutsui

2013

The Journal of Immunology

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The molecular mechanisms of Fas (CD95/Apo-1)-mediated apoptosis are increasingly understood. However, the role of Fas-mediated production of proinflammatory cytokines such as IL-18 and IL-1β in bacterial infection is unclear. We demonstrate the importance of Fas-mediated signaling in IL-18/IL-1β production postinfection with Listeria monocytogenes without the contribution of caspase-1 inflammasome. IL-18/IL-1β production in L. monocytogenes–infected peritoneal exudate cells from Fas-deficient mice was lower than those from wild type mice, indicating that Fas signaling contributes to cytokine production. L. monocytogenes infection induced Fas ligand expression on NK cells, which stimulates Fas expressed on the infected macrophages, leading to the production of IL-18/IL-1β. This was independent of caspase-1, caspase-11, and nucleotide-binding domain and leucine-rich repeat–containing receptors (NLRs) such as Nlrp3 and Nlrc4, but dependent on apoptosis-associated speck-like protein containing a caspase recruitment domain. Wild type cells exhibited caspase-8 activation, whereas Fas-deficient cells did not. L. monocytogenes–induced caspase-8 activation was abrogated by inhibitor for intracellular reactive oxygen species, N-acetyl-L-cysteine. L. monocytogenes–infected macrophages produced type-I IFNs such as IFN-β1, which was required for Il18 gene expression. Thus, Fas signaling regulates innate inflammatory cytokine production in L. monocytogenes infection.

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Section: /2mentioning

confidence: 99%

“…Supernatants of cells stimulated with FasL or infected with L. monocytogenes were concentrated using trichloroacetate (28). Cell lysates were prepared as previously described (28).…”

Section: Detection Of Active Caspase-8mentioning

confidence: 99%

Fas-Mediated Inflammatory Response inListeria monocytogenesInfection

Uchiyama

Yonehara

Tsutsui

2013

The Journal of Immunology

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“…In a third phase, six hours after ConA challenge, the total number of KCs decreases but the remaining KCs have a more potent pro-inflammatory phenotype characterized by high IL-1β secretion [174]. As mentioned before, IL-1β is known as a critical pro-inflammatory cytokine during liver injury [175].…”

Section: Kupffer Cellsmentioning

confidence: 91%

Different Cell Types Involved in Mediating Concanavalin A Induced Liver Injury: A Comprehensive Overview

2016

GHR

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• Concanavalin A (ConA) induced T cell infiltration and liver injury is a model for acute hepatitis• Important cell types include most white blood cells as well as stromal cells• The ConA model has successfully been used to discover new pathways in hepatitis research• New therapeutic interventions for hepatitis were discovered using the ConA model Introduction Autoimmune hepatitisAutoimmune Hepatitis (AIH) is a chronic liver disease associated with raised plasma liver enzymes like transaminases and the presence of autoantibodies [1,2]. The initial trigger of the disease is unknown but different genetic risk factors have been identified [3,4]. In general, it is believed that multiple perturbations, unidentified environmental factors or drugs and the loss of self-tolerance are needed for the onset and development of AIH. The mechanisms for loss of self-tolerance leading to auto reactivity remain unclear but major contributors such as impaired thymic negative selection and expansion of promiscuous T cell clones are suggested [5]. In AIH, presentation of a self-antigen peptide within a Major Histocompatibility (MHC) II molecule by professional Antigen Presenting Cells (APCs) initiates liver damage. This antigen presentation, in combination with exposure to various cytokines, drives the differentiation of uncommitted CD4 helper T cells and immune reaction that is skewed to a Th1 and Th17 response. However, the Th2 response cannot be ignored because it is important in the production of auto-antibodies, which trigger cellular cytotoxicity and complement activation [6,7]. The current standard treatment of AIH patients consists of non-specific immune suppressing drugs such as corticosteroids in combination with azathioprine, which leads to a decrease in serum aminotransferase levels [8]. AIH animal modelsDespite extensive research on the pathogenesis of AIH, the details of the mechanism remain elusive and the current treatments are non-specific and insufficient. The need for faithful and reliable animal models is therefore high. However, finding a suitable animal model is difficult due to the fact that AIH lacks a precise time of onset, etiological agent and the clinical phenotype is variable. According to Czaja et al., the current AIH models can be divided in two categories: the pathogenic and therapeutic models [1]. Pathogenic models focus on characterization of individual mechanisms contributing to occurrence and severity of the disease. In these perturbed models, individual pathways can be isolated and manipulated in a genetic homogenous background. Next to transgenic models in which target antigens are expressed under the control of liver-specific promoters, several inducible models such as the D Galactosamine (GalN) in com HSOA Journal of Gastroenterology & Hepatology Research Review Article AbstractAutoimmune Hepatitis (AIH) is a chronic liver disease where presentation of a self-antigen peptide by professional antigen presenting cells initiates liver damage and drives the differentiation of uncommitted CD4 helpe...

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“…Interestingly, others have reported that the TLR4 TRIF-dependent signaling arm is required for IL-18 production. 10 Through qRT-PCR and flow cytometry, an LPSinduced increase in expression of B7-H1 (B7 homolog 1, also called programmed cell death 1 ligand 1), B7-H2 and, to a lesser extent, CD40 was observed. When assessed in a mixed lymphocyte reaction, LPS treatment imparted an immunosuppressive phenotype on the clonal plasma cells resulting in significantly diminished T-cell proliferation.…”

confidence: 99%

The TOLL of inflammation in multiple myeloma

Bell¹

2011

Cancer Biology & Therapy

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Contribution of TIR domain-containing adapter inducing IFN-β-mediated IL-18 release to LPS-induced liver injury in mice

Cited by 61 publications

References 34 publications

Fas-Mediated Inflammatory Response inListeria monocytogenesInfection

Fas-Mediated Inflammatory Response inListeria monocytogenesInfection

Different Cell Types Involved in Mediating Concanavalin A Induced Liver Injury: A Comprehensive Overview

The TOLL of inflammation in multiple myeloma

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