MYO5B and bile salt export pump contribute to cholestatic liver disorder in microvillous inclusion disease

Muriel Girard, Florence Lacaille, Virginie Verkarre, Raphael Mategot, Gerard Feldmann, Alain Grodet, Frédérique Sauvat, Sabine Irtan, Anne Davit‐Spraul, Emmanuel Jacquemin, Frank Ruemmele, Dominique Rainteau, Olivier Goulet, Virginie Colomb, Christophe Chardot, Alexandra Henrion‐Caude, Dominique Debray – 21 December 2013 – Microvillous inclusion disease (MVID) is a congenital disorder of the enterocyte related to mutations in the MYO5B gene, leading to intractable diarrhea often necessitating intestinal transplantation (ITx).

Serum immunoglobulin G4 and immunoglobulin G1 for distinguishing immunoglobulin G4‐associated cholangitis from primary sclerosing cholangitis

Kirsten Boonstra, Emma L. Culver, Lucas Maillette de Buy Wenniger, Marianne J. Heerde, Karel J. Erpecum, Alexander C. Poen, Karin M.J. Nieuwkerk, B.W. Marcel Spanier, Ben J.M. Witteman, Hans A.R.E. Tuynman, Nan Geloven, Henk Buuren, Roger W. Chapman, Eleanor Barnes, Ulrich Beuers, Cyriel Y.

Mesenchymal stem cell therapy ameliorates diabetic hepatocyte damage in mice by inhibiting infiltration of bone marrow–derived cells

Kanna Nagaishi, Koji Ataka, Eijiro Echizen, Yoshiaki Arimura, Mineko Fujimiya – 21 December 2013 – Although mesenchymal stem cells (MSCs) have been implicated in hepatic injury, the mechanism through which they contribute to diabetic liver disease has not been clarified. In this study, we investigated the effects of MSC therapy on diabetic liver damage with a focus on the role of bone‐marrow–derived cells (BMDCs), which infiltrate the liver, and elucidated the mechanism mediating this process.

Kidney biomarkers and differential diagnosis of patients with cirrhosis and acute kidney injury

Justin M. Belcher, Arun J. Sanyal, Aldo J. Peixoto, Mark A. Perazella, Joseph Lim, Heather Thiessen‐Philbrook, Naheed Ansari, Steven G. Coca, Guadalupe Garcia‐Tsao, Chirag R. Parikh, for the TRIBE‐AKI Consortium – 21 December 2013 – Acute kidney injury (AKI) is common in patients with cirrhosis and associated with significant mortality. The most common etiologies of AKI in this setting are prerenal azotemia (PRA), acute tubular necrosis (ATN), and hepatorenal syndrome (HRS). Accurately distinguishing the etiology of AKI is critical, as treatments differ markedly.

IL‐12/Th1 and IL‐23/Th17 biliary microenvironment in primary biliary cirrhosis: Implications for therapy

Chen‐Yen Yang, Xiong Ma, Koichi Tsuneyama, Shanshan Huang, Toru Takahashi, Naga P. Chalasani, Christopher L. Bowlus, Guo‐Xiang Yang, Patrick S.C. Leung, Aftab A. Ansari, Linda Wu, Ross L. Coppel, M. Eric Gershwin – 21 December 2013 – The interleukin (IL)‐12/IL‐23‐mediated Th1/Th17 signaling pathway has been associated with the etiopathogenesis of primary biliary cirrhosis (PBC).

Cyclosporin A and its analogs inhibit hepatitis B virus entry into cultured hepatocytes through targeting a membrane transporter, sodium taurocholate cotransporting polypeptide (NTCP)

Koichi Watashi, Ann Sluder, Takuji Daito, Satoko Matsunaga, Akihide Ryo, Shushi Nagamori, Masashi Iwamoto, Syo Nakajima, Senko Tsukuda, Katyna Borroto‐Esoda, Masaya Sugiyama, Yasuhito Tanaka, Yoshikatsu Kanai, Hiroyuki Kusuhara, Masashi Mizokami, Takaji Wakita – 21 December 2013 – Chronic hepatitis B virus (HBV) infection is a major public health problem worldwide. Although nucleos(t)ide analogs inhibiting viral reverse transcriptase are clinically available as anti‐HBV agents, emergence of drug‐resistant viruses highlights the need for new anti‐HBV agents interfering with other targets.

Serum immunoglobulin G4 and immunoglobulin G1 for distinguishing immunoglobulin G4‐associated cholangitis from primary sclerosing cholangitis

Kirsten Boonstra, Emma L. Culver, Lucas Maillette de Buy Wenniger, Marianne J. Heerde, Karel J. Erpecum, Alexander C. Poen, Karin M.J. Nieuwkerk, B.W. Marcel Spanier, Ben J.M. Witteman, Hans A.R.E. Tuynman, Nan Geloven, Henk Buuren, Roger W. Chapman, Eleanor Barnes, Ulrich Beuers, Cyriel Y.

Toll‐like receptor 7‐mediated type I interferon signaling prevents cholestasis‐ and hepatotoxin‐induced liver fibrosis

Yoon Seok Roh, Surim Park, Jong Won Kim, Chae Woong Lim, Ekihiro Seki, Bumseok Kim – 21 December 2013 – Toll‐like receptor 7 (TLR7) signaling predominantly regulates production of type I interferons (IFNs), which has been suggested in clinical studies to be antifibrotic. However, the mechanistic role of the TLR7‐type I IFN axis in liver fibrosis has not been elucidated. In the present study, liver fibrosis was induced in wild‐type (WT), TLR7‐deficient, and IFN‐α/β receptor‐1 (IFNAR1)‐deficient mice and TLR7‐mediated signaling was assessed in liver cells isolated from these mice.

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