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Perego J, Bourbon C, Chasson L, et al. Guanabenz Prevents d-Galactosamine/Lipopolysaccharide-Induced Liver Damage and Mortality. Front Immunol. 2017;8:679doi: 10.3389/fimmu.2017.00679.
Perego, J., Bourbon, C., Chasson, L., Laprie, C., Spinelli, L., Camosseto, V., Gatti, E., & Pierre, P. (2017). Guanabenz Prevents d-Galactosamine/Lipopolysaccharide-Induced Liver Damage and Mortality. Frontiers in immunology, 8679. https://doi.org/10.3389/fimmu.2017.00679
Perego, Jessica, et al. "Guanabenz Prevents d-Galactosamine/Lipopolysaccharide-Induced Liver Damage and Mortality." Frontiers in immunology vol. 8 (2017): 679. doi: https://doi.org/10.3389/fimmu.2017.00679
Perego J, Bourbon C, Chasson L, Laprie C, Spinelli L, Camosseto V, Gatti E, Pierre P. Guanabenz Prevents d-Galactosamine/Lipopolysaccharide-Induced Liver Damage and Mortality. Front Immunol. 2017 Jun 13;8:679. doi: 10.3389/fimmu.2017.00679. eCollection 2017. PMID: 28659918; PMCID: PMC5468566.
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Front Immunol. 2017 Jun 13;8:679. doi: 10.3389/fimmu.2017.00679. eCollection 2017.

Guanabenz Prevents d-Galactosamine/Lipopolysaccharide-Induced Liver Damage and Mortality.

Frontiers in immunology

Jessica Perego, Clarisse Bourbon, Lionel Chasson, Caroline Laprie, Lionel Spinelli, Voahirana Camosseto, Evelina Gatti, Philippe Pierre

Affiliations

  1. CIML, Aix-Marseille University, CNRS, INSERM, Marseille, France.
  2. Aveiro Health Sciences Program, Institute for Research in Biomedicine (iBiMED), University of Aveiro, Aveiro, Portugal.
  3. International Associated Laboratory (LIA), CNRS "Mistra", Marseille, France.

PMID: 28659918 PMCID: PMC5468566 DOI: 10.3389/fimmu.2017.00679

Abstract

Multi-organ failure in response to uncontrolled microbial infection is characterized by low blood pressure accompanied by a systemic over-inflammation state, caused by massive pro-inflammatory cytokines release and liver damage. Recently, the integrated stress response (ISR), characterized by eukaryotic translation initiation factor 2α (eIF2α) phosphorylation, was involved with controlling apoptosis in stressed hepatocytes and associated with poor survival to endotoxin challenge. Lipopolysaccharide (LPS) alone is able to induce the ISR in hepatocytes and can trigger massive liver damage along with tumor necrosis factor-alpha (TNF-α) expression. Consequently, drugs interfering with eIF2α phosphorylation may represent potential candidates for the treatment of such pathologies. We, therefore, used Guanabenz (GBZ), a small compound with enhancing eIF2α phosphorylation activity to evaluate its effect on bacterial LPS sensing and endotoxemia. GBZ is confirmed here to have an anti-inflammatory activity by increasing

Keywords: Ppp1r15a; TLR4; guanabenz; lipopolysaccharide-induced liver damage; unfolded protein response

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