Immortalized intrahepatic mouse biliary epithelial cells: Immunologic characterization and immunogenicity

Hreha, Gabriella I.; Jefferson, Douglas M.; Yu, Chunlei; Grubman, Shelley A.; Alsabeh, Randa; Geller, Stephen A.; Vierling, John M.

doi:10.1002/hep.510300216

Cited by 26 publications

(15 citation statements)

References 48 publications

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“…Since EpCAM expression was upregulated in DDC liver, it was examined by IHC using sections of normal liver and of liver from mice fed DDC for 1 or 4 weeks. EpCAM + bile ducts were located adjacent to the portal vein in normal liver as reported previously (de Boer et al, 1999;Hreha et al, 1999;Joplin et al, 1990), whereas there were many EpCAM + cells forming ductular structures away from the portal vein in DDC liver (Fig. 3A).…”

Section: Research Article Hepatic Stem Cells In Adult Liversupporting

confidence: 82%

Potential hepatic stem cells reside in EpCAM+ cells of normal and injured mouse liver

et al. 2009

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Hepatic oval cells are considered to be facultative hepatic stem cells (HSCs) that differentiate into hepatocytes and cholangiocytes in severely injured liver. Hepatic oval cells have also been implicated in tumorigenesis. However, their nature and origin remain elusive. To isolate and characterize mouse oval cells, we searched for cell surface molecules expressed on oval cells and analyzed their nature at the single-cell level by flow cytometric analysis and in the in vitro colony formation assay. We demonstrate that epithelial cell adhesion molecule (EpCAM) is expressed in both mouse normal cholangiocytes and oval cells, whereas its related protein, TROP2, is expressed exclusively in oval cells, establishing TROP2 as a novel marker to distinguish oval cells from normal cholangiocytes.

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Section: Research Article Hepatic Stem Cells In Adult Liversupporting

confidence: 82%

Potential hepatic stem cells reside in EpCAM+ cells of normal and injured mouse liver

et al. 2009

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“…Why CD18-positive neutrophils would kill hepatocytes but not biliary cells after ANIT treatment is uncertain. Hepatocytes and biliary cells upregulate ICAM-1 expression in response to injury (6,8,28,50), and thus both are potential targets of CD18-mediated cytotoxicity (2). It is possible that ICAM-1 is upregulated more strongly on hepatocytes than biliary cells after ANIT treatment.…”

Section: Discussionmentioning

confidence: 99%

ANIT toxicity toward mouse hepatocytes in vivo is mediated primarily by neutrophils via CD18

Kodali¹,

Wu²,

Lahiji³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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. ANIT toxicity toward mouse hepatocytes in vivo is mediated primarily by neutrophils via CD18. Am J Physiol Gastrointest Liver Physiol 291: G355-G363, 2006. First published April 13, 2006 doi:10.1152/ajpgi.00458.2005.-␣-Naphthylisothiocyanate (ANIT) is a hepatotoxicant that causes acute cholestatic hepatitis with infiltration of neutrophils around bile ducts and necrotic hepatocytes. The objective of this study was to determine whether the ␤2-integrin CD18, which plays an important role in leukocyte invasion and cytotoxicity, contributes to ANIT-induced hepatic inflammation and liver injury. Mice with varying levels of leukocyte CD18 expression were treated with ANIT and monitored for hepatic neutrophil influx and liver injury over 48 h. Mice that were partially deficient in CD18 (30% of normal levels) developed periportal inflammation and widespread hepatic necrosis after ANIT treatment in a pattern identical to that in wild-type (WT) mice. In contrast, mice that completely lack CD18 (CD18 null) were resistant to ANIT toxicity. Forty-eight hours after ANIT, CD18-null mice displayed 60% lower serum alanine aminotransferase (ALT) levels and 75% less hepatic necrosis, as shown by morphometry, than WT mice. This was true despite evidence that ANIT still provoked hepatic neutrophil influx in CD18-null mice. WT mice could also be protected from ANIT-induced hepatocellular necrosis, by depleting the animals of neutrophils. Notably, neither CD18-null mice nor neutrophil-depleted WT mice exhibited any attenuation of bile duct injury or cholestasis due to ANIT. We conclude from these experiments that neutrophils invade ANIT-treated livers in a CD18-independent fashion but utilize CD18 to induce hepatocellular cytotoxicity. The results emphasize that neutrophil-mediated amplification of ANIT-induced liver injury is directed toward hepatocytes rather than cholangiocytes. In fact, the data indicate that the majority of ANIT toxicity toward hepatocytes in vivo is neutrophil driven.

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“…Since TGF-beta is also a profibrogenic factor, it seems to be of relevance in hepatic fibrosis associated with chronic hepatitis [44,45]. Several hepatic cell types can function as antigen-presenting cells; T cell stimulation by hepatic antigen presenting cells, which include hepatocytes [46], biliary epithelial cells [47], Kupffer cells [48,49], sinusoidal endothelial cells [49][50][51] and liver dendritic cells [52,53] often results in the induction of non-inflammatory effector T cell responses [54] that may promote chronicity of hepatitis.…”

Section: Acute Vs Chronic Hepatitismentioning

confidence: 98%

Immune-mediated liver injury

Herkel¹,

Schuchmann²,

Tiegs³

et al. 2005

Journal of Hepatology

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Immortalized intrahepatic mouse biliary epithelial cells: Immunologic characterization and immunogenicity

Cited by 26 publications

References 48 publications

Potential hepatic stem cells reside in EpCAM+ cells of normal and injured mouse liver

Potential hepatic stem cells reside in EpCAM+ cells of normal and injured mouse liver

ANIT toxicity toward mouse hepatocytes in vivo is mediated primarily by neutrophils via CD18

Immune-mediated liver injury

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