Ablation of Tumor Necrosis Factor Alpha Receptor 1 Signaling Blunts Steatohepatitis in Peroxisome Proliferator Activated Receptor α-Deficient Mice.

Tumor necrosis factor -alpha (TNFα) is strongly associated with fatty liver disease (i.e, hepatosteatosis). Cytokine production has been thought of as a consequence of hepatic lipid accumulation which becomes a critical factor in the development of chronic liver pathologies as well as insulin resistance.

Analysis of the core bacterial community associated with consumer-ready Eastern oysters (Crassostrea virginica).

Shellfish, such as the Eastern oyster (Crassostrea virginica), are an important agricultural commodity. Previous research has demonstrated the importance of the native microbiome of oysters against exogenous challenges by non-native pathogens. However, the taxonomic makeup of the oyster microbiome and the impact of environmental factors on it are understudied.

Development of a Controlled Laboratory-scale Inoculation System to Study Vibrio parahaemolyticus-oyster Interactions.

Prevalence of seafood-borne gastroenteritis caused by the human pathogen Vibrio parahaemolyticus is increasing globally despite current preventative measures. The United States Centers for Disease Control have designated V. parahaemolyticus as a reportable emerging human pathogen.

Steelhead trout () fed probiotic during the earliest developmental stages have enhanced growth rates and intestinal microbiome bacterial diversity.

Sustainable aquaculture practices can help meet the increasing human demand for seafood, while easing pressures on natural fish populations. Studies aimed at increasing fish production in aquaculture have included supplementary dietary probiotics that often promote general health and enhanced growth rates by altering the microbiome of the host. Steelhead trout () is anadromous, like salmon, and it is a subspecies of rainbow trout capable of rapid growth, making it an attractive fish to the aquaculture industry.

Viral Hepatitis and Hepatocellular Carcinoma: State of the Art.

Viral hepatitis is one of the main causes leading to hepatocellular carcinoma (HCC). The continued rise in incidence of HCC suggests additional factors following infection may be involved. This review examines recent studies investigating the molecular mechanisms of chronic hepatitis and its association with hepatocarcinogenesis.

Adjuvant chemotherapy in curatively resected rectal cancer: How valid are the data?

Background: According to the result of the Cochrane review published in 2012, postoperative adjuvant chemotherapy (CTx) is associated with a survival benefit for rectal cancer patients operated for cure in comparison to patients who underwent only the surgical resection.

Aim: To analyze the quality of the data supporting the advantage of adjuvant CTx after surgery for rectal cancer. In the times of increasing health care costs, it is imperative to offer the patient an evidence-based therapy that justifies potential side effects as well as costs.

Resection or radiofrequency ablation for hepatocellular carcinoma? Assessment of validity of current studies, meta-analyses and their influence on guidelines.

Background: Two Cochrane reviews compared overall survival following liver resection (LR) or radiofrequency ablation (RFA) for patients with hepatocellular carcinoma. The first from 2013, found moderate evidence for a survival advantage for LR over RFA when limiting the analysis to trials at low risk of bias. The second (2017), found no evidence for a difference in all-cause mortality for LR versus RFA.

Impaired T cell-mediated hepatitis in peroxisome proliferator activated receptor alpha (PPARα)-deficient mice.

Background: Peroxisome proliferator activated receptor alpha (PPARα), a regulator of enzymes involved in β oxidation, has been reported to influence lymphocyte activation. The purpose of this study was to determine whether PPARα plays a role in T cell-mediated hepatitis induced by Concanavalin A (ConA).

Methods: Wild type (wt) or PPARα-deficient (PPARα) mice were treated with ConA (15 mg/kg) by intravenous injection 0, 10 or 24 h prior to sacrifice and serum and tissue collection for analysis of tissue injury, cytokine response, T cell activation and characterization.

Iron Status of Vegetarian Adults: A Review of Literature.

The goal of this study was to review published data on iron status among vegetarian adults. Thirteen original articles met the inclusion criteria. Among female vegetarians, the percentage of the sample with ferritin <12 µg/L or <12 ng/mL ranged from 12% to 79%.

Fas Regulates Macrophage Polarization and Fibrogenic Phenotype in a Model of Chronic Ethanol-Induced Hepatocellular Injury.

The role of Fas-mediated apoptosis and its effect on proinflammatory cytokine production in early alcoholic liver disease has not been addressed. Wild-type mice (C57Bl/6) or mice with a functional mutation in the Fas ligand (B6.gld) were given either high-fat control diet or ethanol diet by intragastric cannulation for 2 or 4 weeks.

Fatty acid-binding protein 5 limits the anti-inflammatory response in murine macrophages.

The beginning stages of liver damage induced by various etiologies (i.e. high fat diet, alcohol consumption, toxin exposure) are characterized by abnormal accumulation of lipid in liver.

Alcohol and inflammatory responses: summary of the 2013 Alcohol and Immunology Research Interest Group (AIRIG) meeting.

Loyola University Chicago, Health Sciences Campus in Maywood, Illinois hosted the 18th annual Alcohol and Immunology Research Interest Group (AIRIG) meeting on November 22, 2013. This year's meeting emphasized alcohol's effect on inflammatory responses in diverse disease states and injury conditions. The meeting consisted of three plenary sessions demonstrating the adverse effects of alcohol, specifically, liver inflammation, adverse systemic effects, and alcohol's role in infection and immunology.

Smad3 signaling in the regenerating liver: implications for the regulation of IL-6 expression.

Liver regeneration is vital for graft survival and adequate organ function. Smad activation regulates hepatocyte proliferation and macrophage function. The aim of the current study was to evaluate the impact of Smad3 signaling during liver regeneration in the mouse.

Insulin resistance and metabolic hepatocarcinogenesis with parent-of-origin effects in A×B mice.

Insulin resistance is a defining feature of metabolic syndrome and type 2 diabetes mellitus but also may occur independently of these conditions. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of these disorders, increases the risk of hepatocellular carcinoma (HCC). However, mechanisms linking hyperinsulinemia to NAFLD and HCC require clarification.

Divergent roles of superoxide and nitric oxide in liver ischemia and reperfusion injury.

Liver ischemia and reperfusion-induced injury is a major clinical complication associated with hemorrhagic or endotoxin shock and thermal injury as well as liver transplantation and resectional surgery. Data obtained from several different studies suggest that an important initiating event in the pathophysiology of ischemia and reperfusion-induced tissue injury is enhanced production of superoxide concomitant with a decrease in the bioavailability of endothelial cell-derived nitric oxide. This review will summarize the evidence supporting the hypothesis that the redox imbalance induced by alterations in superoxide and nitric oxide generation creates a more oxidative environment within the different cells of the liver that enhances the nuclear transcription factor-κB-dependent expression of a variety of different cytokines and mediators that may promote as well as limit ischemia and reperfusion-induced hepatocellular injury.

Contribution of gut bacteria to liver pathobiology.

Emerging evidence suggests a strong interaction between the gut microbiota and health and disease. The interactions of the gut microbiota and the liver have only recently been investigated in detail. Receiving approximately 70% of its blood supply from the intestinal venous outflow, the liver represents the first line of defense against gut-derived antigens and is equipped with a broad array of immune cells (i.

Kupffer cell and interleukin-12-dependent loss of natural killer T cells in hepatosteatosis.

Unlabelled: Hepatosteatosis is associated with increased expression of tumor necrosis factor alpha (TNF-alpha) and interleukin (IL)-12, major T helper (Th) 1 cytokines, and reduced hepatic natural killer T (NKT) cell numbers. The relationship between lipid accumulation, cytokine expression, and hepatic NKT cells is not known. This study was conducted to assess the role of IL-12 in the development of hepatic steatosis and its potential impact on liver NKT cells.

Src kinase participates in LPS-induced activation of NADPH oxidase.

The production of superoxide from NADPH oxidase by macrophages in response to endotoxin (LPS) is an important innate immune response, yet it is not clear how LPS signals the activation of NADPH oxidase. The hypothesis is that LPS-induced src kinase and PI3 kinase (PI3K) facilitates the activation of p47(phox), the regulatory subunit of NADPH oxidase. In mouse macrophage RAW264.

Inhibition of phosphatidylinositol 3-kinase signaling in hepatic stellate cells blocks the progression of hepatic fibrosis.

Unlabelled: The hepatic stellate cell (HSC) is the primary cell type in the liver responsible for excess collagen deposition during fibrosis. Following a fibrogenic stimulus the cell changes from a quiescent vitamin A-storing cell to an activated cell type associated with increased extracellular matrix synthesis and increased cell proliferation. The phosphatidylinositol 3-kinase (PI3K) signaling pathway has been shown to regulate several aspects of HSC activation in vitro, including collagen synthesis and cell proliferation.

Mouse model of liver ischemia and reperfusion injury: method for studying reactive oxygen and nitrogen metabolites in vivo.

The mouse model of liver ischemia and reperfusion injury has proven to be valuable for our understanding of the role that reactive oxygen and nitrogen metabolites play in postischemic tissue injury. This methods paper provides a detailed protocol for inducing partial liver ischemia followed by reperfusion. Liver ischemia is induced in anesthetized mice by cross-clamping the hepatic artery and portal vein for varying lengths of time, resulting in deprivation of blood flow to approximately 70% of the liver.

Hepatocellular protection by nitric oxide or nitrite in ischemia and reperfusion injury.

Ischemia and reperfusion (I/R)-induced liver injury occurs in several pathophysiological disorders including hemorrhagic shock and burn as well as resectional and transplantation surgery. One of the earliest events associated with reperfusion of ischemic liver is endothelial dysfunction characterized by the decreased production of endothelial cell-derived nitric oxide (NO). This rapid post-ischemic decrease in NO bioavailability appears to be due to decreased synthesis of NO, enhanced inactivation of NO by the overproduction of superoxide or both.

Accumulation of hedgehog-responsive progenitors parallels alcoholic liver disease severity in mice and humans.

Background & Aims: Improving outcomes in alcoholic liver disease (ALD) necessitates better understanding of how habitual ethanol (EtOH) consumption alters normal regenerative mechanisms within the liver. Hedgehog (Hh) pathway activation promotes expansion of progenitor populations in other tissues. We evaluated the hypothesis that chronic EtOH exposure activates Hh signaling in liver.

Natural killer T cells and non-alcoholic fatty liver disease: fat chews on the immune system.

Natural killer T cells (NKT) are an important subset of T lymphocytes. They are unique in their ability to produce both T helper 1 and T helper 2 associated cytokines, thus being capable of steering the immune system into either inflammation or tolerance. Disruption of NKT cell numbers or function results in severe deficits in immune surveillance against pathogens and tumor cells.