scholarly journals STING‐mediated inflammation contributes to Gao binge ethanol feeding model

2021 ◽  
Author(s):  
Ling Wang ◽  
Hong‐Mei You ◽  
Hong‐Wu Meng ◽  
Xue‐Yin Pan ◽  
Xin Chen ◽  
...  
Keyword(s):  
Ethanol Feeding ◽  
Binge Ethanol

scholarly journals Amelioration of Ethanol-Induced Hepatitis by Magnesium Isoglycyrrhizinate through Inhibition of Neutrophil Cell Infiltration and Oxidative Damage

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Yan Wang ◽  
Zhenzhen Zhang ◽  
Xia Wang ◽  
Dan Qi ◽  
Aijuan Qu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Critical Role ◽  
Flow Cytometric Analysis ◽  
Neutrophil Infiltration ◽  
Cytokines And Chemokines ◽  
Flow Cytometric ◽  
Ethanol Feeding ◽  
Binge Ethanol ◽  
Magnesium Isoglycyrrhizinate

Alcoholic liver disease (ALD) is a leading cause of liver-related morbidity and mortality worldwide. There is no effective treatment to prevent the disease progression. Magnesium isoglycyrrhizinate (MgIG) showed potent anti-inflammatory, antioxidant, and hepatoprotective activities and was used for treating liver diseases in Asia. In this study, we examined whether MgIG could protect mice against alcohol-induced liver injury. The newly developed chronic plus binge ethanol feeding model was used to study the role of MgIG in ALD. Serum liver enzyme levels, H&E staining, immunohistochemical staining, flow cytometric analysis, and real-time PCR were used to evaluate the liver injury and inflammation. We showed that MgIG markedly ameliorated chronic plus binge ethanol feeding liver injury, as shown by decreased serum alanine transaminase and aspartate aminotransferase levels and reduced neutrophil infiltration. The reason may be attributed to the reduced expression of proinflammatory cytokines and chemokines with the treatment of MgIG. The hepatoprotective effect of MgIG was associated with suppression of neutrophil ROS production as well as hepatocellular oxidative stress. MgIG may play a critical role in protecting against chronic plus binge ethanol feeding-induced liver injury by regulating neutrophil activity and hepatic oxidative stress.

scholarly journals TLR2 and TLR9 contribute to alcohol-mediated liver injury through induction of CXCL1 and neutrophil infiltration

2015 ◽  
Vol 309 (1) ◽  
pp. G30-G41 ◽  
Author(s):  
Yoon Seok Roh ◽  
Bi Zhang ◽  
Rohit Loomba ◽  
Ekihiro Seki
Keyword(s):  
Liver Injury ◽  
Alcoholic Hepatitis ◽  
Early Stage ◽  
Neutrophil Infiltration ◽  
Wild Type ◽  
Ethanol Feeding ◽  
Binge Ethanol ◽  
Deficient Mice ◽  
Cxcl1 Expression

Although previous studies reported the involvement of the TLR4-TRIF pathway in alcohol-induced liver injury, the role of TLR2 and TLR9 signaling in alcohol-mediated neutrophil infiltration and liver injury has not been elucidated. Since alcohol binge drinking is recognized to induce more severe form of alcohol liver disease, we used a chronic-binge ethanol-feeding model as a mouse model for early stage of alcoholic hepatitis. Whereas a chronic-binge ethanol feeding induced alcohol-mediated liver injury in wild-type mice, TLR2- and TLR9-deficient mice showed reduced liver injury. Induction of neutrophil-recruiting chemokines, including Cxcl1, Cxcl2, and Cxcl5, and hepatic neutrophil infiltration were increased in wild-type mice, but not in TLR2- and TLR9-deficient mice. In vivo depletion of Kupffer cells (KCs) by liposomal clodronate reduced liver injury and the expression of Il1b, but not Cxcl1, Cxcl2, and Cxcl5, suggesting that KCs are partly associated with liver injury, but not neutrophil recruitment, in a chronic-binge ethanol-feeding model. Notably, hepatocytes and hepatic stellate cells (HSCs) produce high amounts of CXCL1 in ethanol-treated mice. The treatment with TLR2 and TLR9 ligands synergistically upregulated CXCL1 expression in hepatocytes. Moreover, the inhibitors for CXCR2, a receptor for CXCL1, and MyD88 suppressed neutrophil infiltration and liver injury induced by chronic-binge ethanol treatment. Consistent with the above findings, hepatic CXCL1 expression was highly upregulated in patients with alcoholic hepatitis. In a chronic-binge ethanol-feeding model, the TLR2 and TLR9-dependent MyD88-dependent pathway mediates CXCL1 production in hepatocytes and HSCs; the CXCL1 then promotes neutrophil infiltration into the liver via CXCR2, resulting in the development of alcohol-mediated liver injury.

scholarly journals Animals Models of Gastrointestinal and Liver Diseases. Animal models of alcohol-induced liver disease: pathophysiology, translational relevance, and challenges

2014 ◽  
Vol 306 (10) ◽  
pp. G819-G823 ◽  
Author(s):  
Stephanie Mathews ◽  
Mingjiang Xu ◽  
Hua Wang ◽  
Adeline Bertola ◽  
Bin Gao
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
Neutrophil Infiltration ◽  
Alcoholic Liver Injury ◽  
Drinking Patterns ◽  
Excessive Alcohol Consumption ◽  
Ethanol Feeding ◽  
History Of ◽  
Excessive Alcohol ◽  
Binge Ethanol

Over the last four decades, chronic ethanol feeding studies in rodents using either ad libitum feeding or intragastric infusion models have significantly enhanced our understanding of the pathogenesis of alcoholic liver disease (ALD). Recently, we developed a chronic plus binge alcohol feeding model in mice that is similar to the drinking patterns of many alcoholic hepatitis patients: a history of chronic drinking and recent excessive alcohol consumption. Chronic+binge ethanol feeding synergistically induced steatosis, liver injury, and neutrophil infiltration in mice, which may be useful for the study of early alcoholic liver injury and inflammation. Using this chronic+binge model, researchers have begun to identify novel mechanisms that participate in the pathogenesis of alcoholic liver injury, thereby revealing novel therapeutic targets. In this review article, we briefly discuss several mouse models of ALD with a focus on the chronic+binge ethanol feeding model.

scholarly journals Engineered Butyrate-producing Bacillus Subtilis Alleviated Ethanol-induced Intestinal and Liver Damage in Mice

2020 ◽  
Author(s):  
Xing Lu ◽  
Meiqi Zhao ◽  
Yitao Duan ◽  
Fengmei Wang ◽  
Chuanai Chen
Keyword(s):  
Bacillus Subtilis ◽  
Barrier Function ◽  
Circulatory System ◽  
Intestinal Barrier ◽  
Ethanol Exposure ◽  
Intestinal Barrier Function ◽  
Intestinal Dysbiosis ◽  
Ethanol Feeding ◽  
And Function ◽  
Binge Ethanol

Abstract Ethanol-induced intestinal and liver injury are closely associated with intestinal dysbiosis and altered short-chain fatty acid (SCFA) metabolites which is crucial for intestinal health. Bacillus subtilis (BS) strains with biotherapeutic potential can benefit the host through maintaining intestinal homeostasis and regulating systematic immunity via producing small molecules, although these molecules do not include butyrate. To combine the advantages of butyrate and BS, we evaluated the bioactivity of an engineered butyrate-producing Bacillus subtilis (BPBS) strain against ethanol exposure in a chronic-binge ethanol feeding mouse model. Our findings suggested that prophylactic BPBS supplementation restored eubiosis of the gut microbiota and intestinal barrier function, which obviously reduced bacterial translocation of microbial products especially lipopolysaccharide (LPS) to the circulatory system. Additionally, the decrease of serum LPS is responsible for the relief of hepatic inflammation via the Toll-like receptor 4 (TLR4) pathway, resulting in improved hepatic structure and function. Collectively, these results demonstrated that engineered BPBS intervention imparted novel hepatoprotective functions by improving intestinal barrier function and reducing systematic inflammation under ethanol exposure, as well as paving the way for further exploration of engineered probiotics in improving human health care.

Unexpected protective role of the chemokine lix after Gao-binge ethanol feeding in mice

2020 ◽  
Vol 73 ◽  
pp. S189-S190
Author(s):  
Kyle Poulsen ◽  
Christopher Kibler ◽  
Xiude Fan ◽  
Megan McMullen ◽  
Laura Nagy
Keyword(s):  
Protective Role ◽  
Ethanol Feeding ◽  
Binge Ethanol

scholarly journals Interleukin-22 treatment ameliorates alcoholic liver injury in a murine model of chronic-binge ethanol feeding: Role of signal transducer and activator of transcription 3

Hepatology ◽  
2010 ◽  
Vol 52 (4) ◽  
pp. 1291-1300 ◽  
Author(s):  
Sung Hwan Ki ◽  
Oygi Park ◽  
Mingquan Zheng ◽  
Oriol Morales-Ibanez ◽  
Jay K. Kolls ◽  
...  
Keyword(s):  
Liver Injury ◽  
Murine Model ◽  
Alcoholic Liver Injury ◽  
Signal Transducer ◽  
Interleukin 22 ◽  
Ethanol Feeding ◽  
Transcription 3 ◽  
Binge Ethanol

scholarly journals Mouse model of chronic and binge ethanol feeding (the NIAAA model)

2013 ◽  
Vol 8 (3) ◽  
pp. 627-637 ◽  
Author(s):  
Adeline Bertola ◽  
Stephanie Mathews ◽  
Sung Hwan Ki ◽  
Hua Wang ◽  
Bin Gao
Keyword(s):  
Mouse Model ◽  
Ethanol Feeding ◽  
Binge Ethanol
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