Dysbiosis‐induced intestinal inflammation activates tumor necrosis factor receptor I and mediates alcoholic liver disease in mice

Peng Chen, Peter Stärkel, Jerrold R. Turner, Samuel B. Ho, Bernd Schnabl – 24 September 2014 – Intestinal barrier dysfunction is an important contributor to alcoholic liver disease (ALD). Translocated microbial products trigger an inflammatory response in the liver and contribute to steatohepatitis. Our aim was to investigate mechanisms of barrier disruption after chronic alcohol feeding. A Lieber‐DeCarli model was used to induce intestinal dysbiosis, increased intestinal permeability, and liver disease in mice.

Analysis of the intrahepatic ductular reaction and progenitor cell responses in hepatitis C virus recurrence after liver transplantation

Emilia Prakoso, Janina E. E. Tirnitz‐Parker, Andrew D. Clouston, Zeid Kayali, Aimei Lee, Eng K. Gan, Grant A. Ramm, James G. Kench, David G. Bowen, John K. Olynyk, Geoffrey W. McCaughan, Nicholas A. Shackel – 20 September 2014 – Fibrosis in livers with hepatitis C virus (HCV) recurrence after liver transplantation (LT) can be rapidly progressive, and the mechanisms underlying this process are poorly understood.

First description of single‐pass albumin dialysis combined with cytokine adsorption in fulminant liver failure and hemophagocytic syndrome resulting from generalized herpes simplex virus 1 infection

Intestinal ischemic preconditioning ameliorates hepatic ischemia/reperfusion injury in rats: Role of heme oxygenase 1 in the second window of protection

Shoichi Kageyama, Koichiro Hata, Hirokazu Tanaka, Hirofumi Hirao, Toyonari Kubota, Yusuke Okamura, Keiko Iwaisako, Yasutsugu Takada, Shinji Uemoto – 19 September 2014 – Preconditioning by brief ischemia protects not only the concerned organ but also other distant organs against subsequent lethal damage; this is called remote ischemic preconditioning (RIPC). This study was designed to investigate the impact of intestinal RIPC on hepatic ischemia/reperfusion injury (IRI) with a special interest in heme oxygenase 1 (HO‐1) induction in the second window of protection (SWOP).

Liver is the major source of elevated serum lipocalin‐2 levels after bacterial infection or partial hepatectomy: A critical role for IL‐6/STAT3

Ming‐Jiang Xu, Dechun Feng, Hailong Wu, Hua Wang, Yvonne Chan, Jay Kolls, Niels Borregaard, Bo Porse, Thorsten Berger, Tak W. Mak, Jack B. Cowland, Xiaoni Kong, Bin Gao – 18 September 2014 – Lipocalin‐2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase‐associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear.

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