Infections complicating severe alcoholic hepatitis: Enterococcus species represent the most frequently identified pathogen.
Scandinavian Journal of Gastroenterology 51(7):807 (2016)
Patients with acute alcoholic steatohepatitis are at a high risk for infections. To date, neither disease-specific pathogen patterns, nor typical sites of infection, nor antibiotic treatment strategies have been established for AH.
To characterize incidence of infections, pathogen spectrum, site...
Nonalcoholic fatty liver disease is associated with excessive calorie intake rather than a distinctive dietary pattern.
Medicine (Baltimore) 95(23):e3887 (2016)
We aimed to assess the dietary patterns associated with nonalcoholic fatty liver disease (NAFLD) and the efficacy of dietary interventions in a real-life setting at a tertiary medical center in Northern Germany.Clinical and laboratory data as well as data obtained by a semiquantitative food freq...
Arginine and NASH--do macrophages deliver the first hit?
Journal of Hepatology 62(2):260 (2015)
Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue.
Journal of Lipid Research 55(1):104 (2014)
Approximately 80-90% of all retinoids in the body are stored as retinyl esters (REs) in the liver. Adipose tissue also contributes significantly to RE storage. The present studies, employing genetic and nutritional interventions, explored factors that are responsible for regulating RE accumulati...
Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice.
Hepatology 58(4):1461 (2013)
Although it is well established that hepatic macrophages play a crucial role in the development of liver fibrosis, the underlying mechanisms remain largely elusive. Moreover, it is not known whether other mononuclear phagocytes such as dendritic cells (DCs) contribute to hepatic stellate cell (H...
Induction of heme oxygenase 1 prevents progression of liver fibrosis in Mdr2 knockout mice.
Hepatology 55(2):553 (2012)
Induction or overexpression of the heme-degrading enzyme, heme oxygenase 1 (HO-1), has been shown to protect mice from liver damage induced by acute inflammation. We have investigated the effects of HO-1 induction in a mouse model of chronic liver inflammation and fibrogenesis with progression t...
Absence of hepatic stellate cell retinoid lipid droplets does not enhance hepatic fibrosis but decreases hepatic carcinogenesis.
Gut 60(9):1260 (2011)
Hepatic stellate cells (HSCs) contain a number of bioactive metabolites or their precursors including retinoids in their characteristic lipid droplets. The loss of lipid droplets and retinoids is a hallmark of HSC activation, but it remains unclear whether this loss promotes HSC activation, live...
Role and cellular source of nicotinamide adenine dinucleotide phosphate oxidase in hepatic fibrosis.
Hepatology 52(4):1420 (2010)
Reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate oxidase (NOX) is required for liver fibrosis. This study investigates the role of NOX in ROS production and the differential contribution of NOX from bone marrow (BM)-derived and non-BM-derived liver cells. He...
Modulation of hepatic fibrosis by c-Jun-N-terminal kinase inhibition.
Gastroenterology 138(1):347 (2010)
c-Jun N-terminal kinase (JNK) is activated by multiple profibrogenic mediators; JNK activation occurs during toxic, metabolic, and autoimmune liver injury. However, its role in hepatic fibrogenesis is unknown.
JNK phosphorylation was detected by immunoblot analysis and confocal immunofluorescent...
Angiotensin-converting-enzyme 2 inhibits liver fibrosis in mice.
Hepatology 50(3):929 (2009)
The renin-angiotensin system (RAS) plays a major role in liver fibrosis. Recently, a homolog of angiotensin-converting-enzyme 1 (ACE1), termed ACE2, has been identified that appears to be a negative regulator of the RAS by degrading Ang II to Ang(1-7). The aim of this study was to characterize t...
CCR1 and CCR5 promote hepatic fibrosis in mice.
Journal of Clinical Investigation 119(7):1858 (2009)
Hepatic fibrosis develops as a response to chronic liver injury and almost exclusively occurs in a proinflammatory environment. However, the role of inflammatory mediators in fibrogenic responses of the liver is only poorly understood. We therefore investigated the role of CC chemokines and thei...
Hepatic stellate cell lipid droplets: a specialized lipid droplet for retinoid storage.
Biochimica et Biophysica Acta 1791(6):467 (2009)
The majority of retinoid (vitamin A and its metabolites) present in the body of a healthy vertebrate is contained within lipid droplets present in the cytoplasm of hepatic stellate cells (HSCs). Two types of lipid droplets have been identified through histological analysis of HSCs within the liv...
Toll-like receptors, wound healing, and carcinogenesis.
Klinische Wochenschrift 87(2):125 (2009)
Following acute injury, the concerted action of resident and nonresident cell populations evokes wound healing responses that entail a temporary increase in inflammation, extracellular matrix production, and proliferation to ultimately restore normal organ architecture. However, chronic injury e...
535 JNK1, But Not JNK2 Promotes Hepatic Fibrogenesis
Gastroenterology 136(5):A (2009)
M1580 Loss of Hepatic Stellate Cell Lipid Droplets Does Not Contribute to Stellate Cell Activation and Liver Fibrosis
Gastroenterology 134(4):A (2008)
TLR4 enhances TGF-beta signaling and hepatic fibrosis.
Nature Medicine 13(11):1324 (2007)
Hepatic injury is associated with a defective intestinal barrier and increased hepatic exposure to bacterial products. Here we report that the intestinal bacterial microflora and a functional Toll-like receptor 4 (TLR4), but not TLR2, are required for hepatic fibrogenesis. Using Tlr4-chimeric mi...
Gene expression profiles during hepatic stellate cell activation in culture and in vivo.
Gastroenterology 132(5):1937 (2007)
Following hepatic injury, hepatic stellate cells (HSCs) transdifferentiate to become extracellular matrix-producing myofibroblasts and to promote hepatic fibrogenesis. In this study, we determine gene expression changes in 3 different models of HSC activation and investigate whether HSC culture ...
Gene Expression Profiles During Hepatic Stellate Cell Activation in Culture and In Vivo
Gastroenterology 132(5):1937 (2007)
Background & Aims:
Following hepatic injury, hepatic stellate cells (HSCs) transdifferentiate to become extracellular matrix-producing myofibroblasts and to promote hepatic fibrogenesis. In this study, we determine gene expression changes in 3 different models of HSC a...