Immune-mediated Liver Injury in Hepatitis B Virus Infection

Oh, In Soo; Park, Su–Hyung

doi:10.4110/in.2015.15.4.191

Cited by 56 publications

(34 citation statements)

References 81 publications

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“…Acute liver injury is a kind of abnormal liver function caused by many factors such as virus infection, improper use of drugs, excessive intake of alcohol, ingestion of toxic food, trauma, and radiation damage . Liver injury is the basis of acute liver failure, and severe or persistent liver injury will eventually lead to liver failure.…”

Section: Introductionmentioning

confidence: 99%

Hepatoprotective effect of chiisanoside from Acanthopanax sessiliflorus against LPS/D‐GalN‐induced acute liver injury by inhibiting NF‐κB and activating Nrf2/HO‐1 signaling pathways

Bian

Liu

et al. 2019

J Sci Food Agric

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BACKGROUND In China, Acanthopanax sessiliflorus is a delicious wild vegetable. It is also used to treat inflammation and pain. Chiisanoside (CSS) is the main constituent of the leaf of A. sessiliflorus. Combined use of lipopolysaccharide and d‐galactosamine (LPS/D‐GalN) can induce acute liver failure in human beings, and there are no reports on the protective effect of CSS against LPS/D‐GalN‐induced acute liver injury in mice. RESULTS Chiisanoside pretreatment evidently reduced the activities of alanine transaminase (ALT) and aspartate transaminase (AST) in the changes induced by LPS/D‐GalN, and these histopathological changes induced by LPS/GalN were significantly weakened. Catalase (CAT), glutathione (GSH), and superoxide dismutase (SOD) activities increased, and malondialdehyde (MDA) activity decreased after CSS treatment compared with LPS/D‐GalN treatment. Pretreatment with CSS also inhibited the expression levels of inflammatory factors. The administration of CSS prevented the phosphorylated expression of inhibitor kappa B (IκB) kinase, and led to a significant increase in heme oxygenase‐1 (HO‐1) expression and nuclear factor erythroid 2‐related factor2 (Nrf2) nuclear translocation. CONCLUSION The protective effects of CSS are attributed to its antioxidative effect and inflammatory suppression in Nuclear factor kappa beta (NF‐κB) and Nrf2/HO‐1 signaling pathways. Chiisanoside might therefore be a potential ingredient for drug and food development against acute liver injury in the future. © 2018 Society of Chemical Industry

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Section: Introductionmentioning

confidence: 99%

Hepatoprotective effect of chiisanoside from Acanthopanax sessiliflorus against LPS/D‐GalN‐induced acute liver injury by inhibiting NF‐κB and activating Nrf2/HO‐1 signaling pathways

Bian

Liu

et al. 2019

J Sci Food Agric

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“…Acute liver injury is a liver function abnormality that results from multiple reasons, such as viral infection, abuse of drugs or alcohol, ingestion of toxic substance and so on [1,2]. Serious or continuous liver injury often gives rise to liver cirrhosis or liver failure and results in death.…”

Section: Introductionmentioning

confidence: 99%

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting the autophagy in mice

Han¹,

Shi²,

Duan³

2017

Journal of Hepatology

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“…Viral infection and liver damage is often exacerbated through cytokine storm and immune dysregulation (39)(40)(41). Having shown that the IFN status of the immune compartment is critical for controlling generalized infections and liver damage, we sought to assess whether abnormal cytokine levels were an additional component in the liver disease observed in IFN-␣␤␥R Ϫ/Ϫ mice.…”

Section: Ifn-␣␤␥rmentioning

confidence: 99%

Immune- and Nonimmune-Compartment-Specific Interferon Responses Are Critical Determinants of Herpes Simplex Virus-Induced Generalized Infections and Acute Liver Failure

Parker

Pasieka

Parker

et al. 2016

J Virol

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The interferon (IFN) response to viral pathogens is critical for host survival. In humans and mouse models, defects in IFN responses can result in lethal herpes simplex virus 1 (HSV-1) infections, usually from encephalitis. Although rare, HSV-1 can also cause fulminant hepatic failure, which is often fatal. Although herpes simplex encephalitis has been extensively studied, HSV-1 generalized infections and subsequent acute liver failure are less well understood. We previously demonstrated that IFN- IMPORTANCEHerpes simplex virus 1 (HSV-1) infection is an incurable viral infection with the most significant morbidity and mortality occurring in neonates and patients with compromised immune systems. Severe pathologies from HSV include the blindness-inducing herpetic stromal keratitis, highly debilitating and lethal herpes simplex encephalitis, and generalized infections that can lead to herpes simplex virus-induced acute liver failure. While immune compromise is a known factor, the precise mechanisms that lead to generalized HSV infections are unknown. In this study, we used and developed a mouse model system in combination with real-time bioluminescence imaging to demonstrate the relative importance of the immune and nonimmune compartments for containing viral spread and promoting host survival after corneal infection. Our results shed light on the pathogenesis of HSV infections that lead to generalized infection and acute liver failure. Herpes simplex virus 1 (HSV-1) is an enveloped DNA virus and a member of the Alphaherpesvirus subfamily with high seroprevalence in the human population (1). In most cases, HSV-1 causes relatively mild orolabial cold sores, but it can cause more serious localized diseases such herpes stromal keratitis, the leading cause of infectious blindness in the United States (2, 3). Serious sequelae for HSV-1 are more common in immunocompromised hosts and neonates, with uncontrolled viral replication leading to herpes simplex encephalitis (HSE) or, more rarely, HSV sepsis leading to acute liver failure (4, 5). HSV-induced acute liver failure (ALF) is an alarmingly deadly disease with a lethality rate approaching 75% (5). The importance of studying HSV-induced ALF is underscored by the immunocompromised populations it affects, mainly patients undergoing chemotherapy, bone marrow transplant recipients, HIV patients, and women in the third trimester of pregnancy (5, 6). HSV-1 infects via the mucosae of the mouth, eyes, or genitalia, where it undergoes lytic replication in the epithelium (7). During infection of these mucosae, the virus infects innervating sensory neurons, traveling in a retrograde direction in the facial neurons back to mostly sensory ganglia, wherein HSV-1 establishes latency (8). The ability of HSV to establish latency in neurons, a nondividing cell population, hinders the ability of the immune system to fully clear the virus and renders the virus refractory to cure with antiviral treatments (9). Immune dysregulation and other stimuli cause HSV-1 to erupt from latency,...

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Immune-mediated Liver Injury in Hepatitis B Virus Infection

Cited by 56 publications

References 81 publications

Hepatoprotective effect of chiisanoside from Acanthopanax sessiliflorus against LPS/D‐GalN‐induced acute liver injury by inhibiting NF‐κB and activating Nrf2/HO‐1 signaling pathways

Hepatoprotective effect of chiisanoside from Acanthopanax sessiliflorus against LPS/D‐GalN‐induced acute liver injury by inhibiting NF‐κB and activating Nrf2/HO‐1 signaling pathways

Augmenter of liver regeneration protects against carbon tetrachloride-induced liver injury by promoting the autophagy in mice

Immune- and Nonimmune-Compartment-Specific Interferon Responses Are Critical Determinants of Herpes Simplex Virus-Induced Generalized Infections and Acute Liver Failure

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