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Full-Text Articles in Hepatology
Gut Microbial Trimethylamine Is Elevated In Alcohol-Associated Hepatitis And Contributes To Ethanol-Induced Liver Injury In Mice, Robert N. Helsley, Tatsunori Miyata, Anagha Kadam, Venkateshwari Varadharajan, Naseer Sangwan, Emily C. Huang, Rakhee Banerjee, Amanda L. Brown, Kevin K. Fung, William J. Massey, Chase Neumann, Danny Orabi, Lucas J. Osborn, Rebecca C. Schugar, Megan R. Mcmullen, Annette Bellar, Kyle L. Poulsen, Adam Kim, Vai Pathak, Marko Mrdjen
Gut Microbial Trimethylamine Is Elevated In Alcohol-Associated Hepatitis And Contributes To Ethanol-Induced Liver Injury In Mice, Robert N. Helsley, Tatsunori Miyata, Anagha Kadam, Venkateshwari Varadharajan, Naseer Sangwan, Emily C. Huang, Rakhee Banerjee, Amanda L. Brown, Kevin K. Fung, William J. Massey, Chase Neumann, Danny Orabi, Lucas J. Osborn, Rebecca C. Schugar, Megan R. Mcmullen, Annette Bellar, Kyle L. Poulsen, Adam Kim, Vai Pathak, Marko Mrdjen
Pediatrics Faculty Publications
There is mounting evidence that microbes residing in the human intestine contribute to diverse alcohol-associated liver diseases (ALD) including the most deadly form known as alcohol-associated hepatitis (AH). However, mechanisms by which gut microbes synergize with excessive alcohol intake to promote liver injury are poorly understood. Furthermore, whether drugs that selectively target gut microbial metabolism can improve ALD has never been tested. We used liquid chromatography tandem mass spectrometry to quantify the levels of microbe and host choline co-metabolites in healthy controls and AH patients, finding elevated levels of the microbial metabolite trimethylamine (TMA) in AH. In subsequent studies, we …
Complement Factor D Protects Mice From Ethanol-Induced Inflammation And Liver Injury., Rebecca L Mccullough, Megan R Mcmullen, Megan M Sheehan, Kyle L Poulsen, Sanjoy Roychowdhury, Dian J Chiang, Michele T Pritchard, Juan Caballeria, Laura E Nagy
Complement Factor D Protects Mice From Ethanol-Induced Inflammation And Liver Injury., Rebecca L Mccullough, Megan R Mcmullen, Megan M Sheehan, Kyle L Poulsen, Sanjoy Roychowdhury, Dian J Chiang, Michele T Pritchard, Juan Caballeria, Laura E Nagy
Articles, Abstracts, and Reports
Complement plays a crucial role in microbial defense and clearance of apoptotic cells. Emerging evidence suggests complement is an important contributor to alcoholic liver disease. While complement component 1, Q subcomponent (C1q)-dependent complement activation contributes to ethanol-induced liver injury, the role of the alternative pathway in ethanol-induced injury is unknown. Activation of complement via the classical and alternative pathways was detected in alcoholic hepatitis patients. Female C57BL/6J [wild type (WT)], C1q-deficient ( C1qa
Chronic Alcohol-Induced Microrna-155 Contributes To Neuroinflammation In A Tlr4-Dependent Manner In Mice, Dora Lippai, Shashi Bala, Timea Csak, Evelyn A. Kurt-Jones, Gyongyi Szabo
Chronic Alcohol-Induced Microrna-155 Contributes To Neuroinflammation In A Tlr4-Dependent Manner In Mice, Dora Lippai, Shashi Bala, Timea Csak, Evelyn A. Kurt-Jones, Gyongyi Szabo
Gyongyi Szabo
INTRODUCTION: Alcohol-induced neuroinflammation is mediated by pro-inflammatory cytokines and chemokines including tumor necrosis factor-alpha (TNFalpha), monocyte chemotactic protein-1 (MCP1) and interleukin-1-beta (IL-1beta). Toll-like receptor-4 (TLR4) pathway induced nuclear factor-kappaB (NF-kappaB) activation is involved in the pathogenesis of alcohol-induced neuroinflammation. Inflammation is a highly regulated process. Recent studies suggest that microRNAs (miRNAs) play crucial role in fine tuning gene expression and miR-155 is a major regulator of inflammation in immune cells after TLR stimulation. AIM: To evaluate the role of miR-155 in the pathogenesis of alcohol-induced neuroinflammation. METHODS: Wild type (WT), miR-155- and TLR4-knockout (KO) mice received 5% ethanol-containing or isocaloric …