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Journal articles on the topic 'Biliary epithelium'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Alpini, G., R. Lenzi, W. R. Zhai, P. A. Slott, M. H. Liu, L. Sarkozi, and N. Tavoloni. "Bile secretory function of intrahepatic biliary epithelium in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 1 (July 1, 1989): G124—G133. http://dx.doi.org/10.1152/ajpgi.1989.257.1.g124.

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To shed light on ductular fluid secretion, hepatic histology and ultrastructure, cell proliferation and phenotypes, and several aspects of biliary physiology were studied in rats with ductular cell hyperplasia induced by either biliary obstruction (0-14 days) or 1-naphthylisothiocyanate (ANIT) feeding (0-28 days). In both groups of experimental animals, bile duct hyperplasia and spontaneous bile flow and secretin-induced choleresis increased with time of treatment in a linear fashion. Measurements of [14C]mannitol biliary entry and of biliary tree volume showed that the increase in both spontaneous and secretin-stimulated bile flow originated at the proliferated biliary structures. Ultrastructural examination, [3H]thymidine incorporation, and histochemical and immunohistochemical staining for various markers demonstrated that in both hyperplastic reactions the proliferated cells were the progeny of preexisting biliary epithelial cells and retained their characteristics. These results indicate that the increased bile secretory activity associated with either biliary obstruction or ANIT intoxication reflects a quantitative change due to the proliferation of biliary epithelial cells. Thus both models of bile ductular cell hyperplasia lend themselves to assessment of the transport function of intrahepatic biliary epithelium and its contribution to normal bile formation. In the present studies, we have estimated that net ductular secretion in the normal rat accounts for 10-13% of spontaneously secreted hepatic bile.

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2

Katabi, Nora. "Neoplasia of Gallbladder and Biliary Epithelium." Archives of Pathology & Laboratory Medicine 134, no. 11 (November 1, 2010): 1621–27. http://dx.doi.org/10.5858/2009-0580-rar.1.

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Abstract Context.—Diagnosis of biliary neoplasia can be challenging but is essential for the appropriate clinical management of patients. Therefore, it is important to recognize the morphologic features of the biliary neoplasms to report a correct diagnosis. Objectives.—(1) To discuss the differential diagnosis of dysplasia in the gallbladder and differentiate dysplasia from reactive atypia and invasive carcinoma, (2) review the histologic features of adenoma and polypoid biliary lesions, (3) highlight the differential diagnosis of adenocarcinoma in liver biopsy, and (4) discuss the differential diagnosis of atypical biliary glandular lesions. Data Sources.—Current English literature related to gallbladder and biliary neoplasia. Conclusions.—Biliary glandular neoplasms show a wide spectrum of morphology and have many mimics. Careful examination of the histologic features of these lesions and familiarity with their morphology can help to achieve the correct diagnosis.

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3

Fava, Giammarco, Shannon Glaser, Heather Francis, and Gianfranco Alpini. "The Immunophysiology of Biliary Epithelium." Seminars in Liver Disease 25, no. 03 (August 2005): 251–64. http://dx.doi.org/10.1055/s-2005-916318.

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4

Nguyen, N. Thao T., Theresa R. Harring, Laurie Holley, John A. Goss, and Christine A. O’Mahony. "Biliary Adenofibroma with Carcinoma In Situ: A Rare Case Report." Case Reports in Hepatology 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/793963.

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This case report exhibits a rare biliary tumor within the liver of a 53-year-old Caucasian woman. This exophytic, multicystic, 6.5×5.0 cm mass was composed of complex tubulocystic structures lined by nonmucin-secreting, biliary epithelium embedded in fibrous stroma, consistent with biliary adenofibroma. This is the seventh case described in the literature. Multiple foci of high-grade dysplasia/carcinoma in situ were found with a microscopic focus of invasive carcinoma in review of the pathology, making this only the second case reporting malignant transformation. It is presented to illustrate the premalignant potential in a biliary epithelial tumor currently categorized as benign.

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5

Li, Daneng, Ya-Han Zhang, Christiana J. Crook, and Renuka V. Iyer. "Updates in Biliary Tract Cancers." Cancers 14, no. 11 (June 1, 2022): 2746. http://dx.doi.org/10.3390/cancers14112746.

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6

Park, Ji-Won, Jung-Hee Kim, Sung-Eun Kim, Jang Han Jung, Myoung-Kuk Jang, Sang-Hoon Park, Myung-Seok Lee, Hyoung-Su Kim, Ki Tae Suk, and Dong Joon Kim. "Primary Biliary Cholangitis and Primary Sclerosing Cholangitis: Current Knowledge of Pathogenesis and Therapeutics." Biomedicines 10, no. 6 (May 31, 2022): 1288. http://dx.doi.org/10.3390/biomedicines10061288.

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Cholangiopathies encompass various biliary diseases affecting the biliary epithelium, resulting in cholestasis, inflammation, fibrosis, and ultimately liver cirrhosis. Primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC) are the most important progressive cholangiopathies in adults. Much research has broadened the scope of disease biology to genetic risk, epigenetic changes, dysregulated mucosal immunity, altered biliary epithelial cell function, and dysbiosis, all of which interact and arise in the context of ill-defined environmental triggers. An in-depth understanding of the molecular pathogenesis of these cholestatic diseases will help clinicians better prevent and treat diseases. In this review, we focus on the main underlying mechanisms of disease initiation and progression, and novel targeted therapeutics beyond currently approved treatments.

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7

Glaser, Shannon. "Heterogeneity of the intrahepatic biliary epithelium." World Journal of Gastroenterology 12, no. 22 (2006): 3523. http://dx.doi.org/10.3748/wjg.v12.i22.3523.

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8

Strazzabosco, Mario, Carlo Spirlì, and Lajos Okolicsanyi. "Pathophysiology of the intrahepatic biliary epithelium." Journal of Gastroenterology and Hepatology 15, no. 3 (March 10, 2000): 244–53. http://dx.doi.org/10.1046/j.1440-1746.2000.02091.x.

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9

Morell, Carola M., Luca Fabris, and Mario Strazzabosco. "Vascular biology of the biliary epithelium." Journal of Gastroenterology and Hepatology 28 (July 15, 2013): 26–32. http://dx.doi.org/10.1111/jgh.12022.

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10

Allen, Steven R., Mubeen Jafri, Bryan Donnelly, Monica McNeal, David Witte, Jorge Bezerra, Richard Ward, and Gregory M. Tiao. "Effect of Rotavirus Strain on the Murine Model of Biliary Atresia." Journal of Virology 81, no. 4 (November 22, 2006): 1671–79. http://dx.doi.org/10.1128/jvi.02094-06.

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ABSTRACT Biliary atresia is a devastating disorder of the newborn in which afflicted infants develop inflammation and fibrosis of the extrahepatic biliary tract, resulting in cirrhosis and end-stage liver disease. Infection with a virus is thought to be a contributing factor in the etiology of biliary atresia. In the murine model of biliary atresia, perinatal exposure to rhesus rotavirus (RRV) results in biliary epithelial cell infection causing bile duct obstruction. The purpose of this study was to determine if tropism for the biliary epithelial cell was unique to RRV. Newborn mice underwent intraperitoneal injection with five strains of rotavirus: RRV (simian), SA11-FM (simian/bovine), SA11-SM (simian), EDIM (murine), and Wa (human). RRV and SA11-FM caused clinical manifestations of bile duct obstruction and high mortality. SA11-SM caused clinical signs of hepatobiliary injury but the mortality was markedly reduced. EDIM and Wa caused no sign of hepatobiliary disease. The systemic and temporal distribution of viral protein and live virus varied according to the injected strain. Immunohistochemistry revealed that RRV and SA11-FM targeted the biliary epithelial cells. In contrast, SA11-SM was found in the liver but in not in the biliary epithelium. These results indicate that strain-specific characteristics dictate tropism for cells of hepatobiliary origin which in turn impact the ability to induce the murine model of biliary atresia.

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11

Terada, T., N. Kono, and Y. Nakanuma. "Immunohistochemical and immunoelectron microscopic analyses of alpha-amylase isozymes in human intrahepatic biliary epithelium and hepatocytes." Journal of Histochemistry & Cytochemistry 40, no. 11 (November 1992): 1627–35. http://dx.doi.org/10.1177/40.11.1431051.

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The expression and localization of the pancreatic and salivary isozymes of alpha-amylase in the intrahepatic biliary epithelium and hepatocytes were examined by the immunohistochemical method with polyclonal and monoclonal antibodies in 45 normal autopsied human livers. Immunoelectron microscopic studies with the protein A-gold method were performed with the monoclonal antibodies (MAb) on seven of the livers. The intrahepatic biliary system was divided into large ducts, septal ducts, interlobular ducts, bile ductules, and peribiliary glands. Immunohistochemically, pancreatic isozyme was observed in the supranuclear cytoplasm of the epithelium of large ducts, septal ducts, and peribiliary glands in almost all livers. Interlobular ducts expressed pancreatic isozyme in only four (9%) livers. Bile ductules and hepatocytes were negative for pancreatic isozyme in all cases. Expression of salivary isozyme was observed in the supranuclear cytoplasm of the epithelium of large ducts, septal ducts, interlobular ducts, bile ductules, and peribiliary glands in almost all livers, although the expression in interlobular ducts and bile ductules was weak. Hepatocytes were weakly positive for salivary isozyme. Immunoelectron microscopy revealed that both pancreatic and salivary isozymes were located in the supranuclear cytoplasm of the epithelium of large ducts, septal ducts, and peribiliary glands, and that hepatocytes had no pancreatic isozyme but contained salivary isozyme. These data suggest that pancreatic and salivary isozymes of alpha-amylase are produced by the intrahepatic biliary epithelium and secreted into intrahepatic biliary lumens, and that they may play an important role in the physiology of the intrahepatic biliary tree and hepatic bile. It is also suggested that hepatocytes produce a small amount of salivary alpha-amylase that may be secreted into the biliary tree.

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12

Marucci, L., L. Ugili, G. Macarri, G. Feliciangeli, E. Bendia, A. M. Jezequel, F. Orlandi, and A. Benedetti. "Primary biliary cirrhosis: modalities of injury and death in biliary epithelium." Digestive and Liver Disease 33, no. 7 (October 2001): 576–83. http://dx.doi.org/10.1016/s1590-8658(01)80110-9.

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13

Etherington, R. E., B. Millar, B. Innes, J. Brain, J. Kirby, and D. Jones. "T cell interactions with the biliary epithelium in primary biliary cholangitis." Journal of Hepatology 66, no. 1 (2017): S553—S554. http://dx.doi.org/10.1016/s0168-8278(17)31519-2.

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14

Coad, R. A., J. R. Dutton, D. Tosh, and J. M. W. Slack. "Inhibition of Hes1 activity in gall bladder epithelial cells promotes insulin expression and glucose responsiveness." Biochemistry and Cell Biology 87, no. 6 (December 2009): 975–87. http://dx.doi.org/10.1139/o09-063.

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The biliary system has a close developmental relationship with the pancreas, evidenced by the natural occurrence of small numbers of biliary-derived β-cells in the biliary system and by the replacement of biliary epithelium with pancreatic tissue in mice lacking the transcription factor Hes1. In normal pancreatic development, Hes1 is known to repress endocrine cell formation. Here we show that glucose-responsive insulin secretion can be induced in biliary epithelial cells when activity of the transcription factor Hes1 is antagonised. We describe a new culture system for adult murine gall bladder epithelial cells (GBECs), free from fibroblast contamination. We show that Hes1 is expressed both in adult murine gall bladder and in cultured GBECs. We have created a new dominant negative Hes1 (ΔHes1) by removal of the DNA-binding domain, and show that it antagonises Hes1 function in vivo. When ΔHes1 is introduced into the GBEC it causes expression of insulin RNA and protein. Furthermore, it confers upon the cells the ability to secrete insulin following exposure to increased external glucose. GBEC cultures are induced to express a wider range of mature β cell markers when co-transduced with ΔHes1 and the pancreatic transcription factor Pdx1. Introduction of ΔHes1 and Pdx1 can therefore initiate a partial respecification of phenotype from biliary epithelial cell towards the pancreatic β cell.

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15

Seo, Dong Wan, Ho-Soon Choi, Sum P. Lee, and Rahul Kuver. "Oxysterols from human bile induce apoptosis of canine gallbladder epithelial cells in monolayer culture." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 6 (December 2004): G1247—G1256. http://dx.doi.org/10.1152/ajpgi.00013.2004.

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Oxysterols have been detected in various mammalian organs and blood. Biliary epithelium is exposed to high concentrations of cholesterol, and we have identified three keto-oxysterols (cholest-4-en-3-one, cholesta-4,6-dien-3-one, cholesta-3,5-dien-7-one) in human bile and gallstones. Because the effects of oxysterols on biliary physiology are not well defined, we investigated their biological effects on dog gallbladder epithelial cells. Enriched medium (culture medium containing taurocholate and lecithin and cholesterol ± various oxysterols) was applied to confluent monolayers of dog gallbladder epithelial cells in culture. Cytotoxicity and apoptosis were studied by morphological analysis and flow cytometry. Oxysterols in the mitochondrial fraction were identified by gas chromatography/mass spectrometry, whereas release of cytochrome c from mitochondria was assayed by spectrophotometry and Western blot analysis. Compared with cells treated with culture medium or with enriched medium containing cholesterol, oxysterol-treated cells showed significantly increased apoptosis ( P < 0.05). Exogenously applied oxysterols were recovered from the mitochondrial fraction. Cytochrome c release from mitochondria was increased significantly by cholest-4-en-3-one, cholesta-4,6-dien-3-one, and 5β-cholestan-3-one (all P < 0.05). Thus oxysterols recovered from human bile and gallstones induce apoptosis of biliary epithelium via a mitochondrial-dependent pathway and may play a role in the pathogenesis of chronic inflammation and carcinogenesis in the gallbladder.

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16

Chuang, Ya-Hui, Ruth Y. Lan, and M. Eric Gershwin. "The immunopathology of human biliary cell epithelium." Seminars in Immunopathology 31, no. 3 (June 17, 2009): 323–31. http://dx.doi.org/10.1007/s00281-009-0172-5.

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17

Reynoso-Paz, Sandra, Ross L. Coppel, Ian R. Mackay, Nathan M. Bass, Aftab A. Ansari, and M. Eric Gershwin. "The immunobiology of bile and biliary epithelium." Hepatology 30, no. 2 (August 1999): 351–57. http://dx.doi.org/10.1002/hep.510300218.

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18

Kanno, Noriatsu, Gene LeSage, Shannon Glaser, Domenico Alvaro, and Gianfranco Alpini. "Functional heterogeneity of the intrahepatic biliary epithelium." Hepatology 31, no. 3 (March 2000): 555–61. http://dx.doi.org/10.1002/hep.510310302.

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19

Alshbib, Ayham, Krzysztof Grzyb, Trygve Syversveen, Henrik Mikael Reims, Kristoffer Lassen, and Sheraz Yaqub. "Biliary Adenofibroma: A Rare Liver Tumor with Transition to Invasive Carcinoma." Case Reports in Surgery 2022 (February 7, 2022): 1–5. http://dx.doi.org/10.1155/2022/5280884.

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Biliary adenofibroma is a rare benign liver tumor with potential for malignant transition. It has a bile duct origin characterized by a complex tubulocystic biliary epithelium with fibrous stroma. MRI features may suggest this uncommon entity, and histological findings can be diagnostic. We report a case of biliary adenofibroma with transformation to an intrahepatic cholangiocarcinoma.

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20

Dutta, Amal K., Al-karim Khimji, Meghana Sathe, Charles Kresge, Vinay Parameswara, Victoria Esser, Don C. Rockey, and Andrew P. Feranchak. "Identification and functional characterization of the intermediate-conductance Ca2+-activated K+ channel (IK-1) in biliary epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 5 (November 2009): G1009—G1018. http://dx.doi.org/10.1152/ajpgi.00223.2009.

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In the liver, adenosine triphosphate (ATP) is an extracellular signaling molecule that is released into bile and stimulates a biliary epithelial cell secretory response via engagement of apical P2 receptors. The molecular identities of the ion channels involved in ATP-mediated secretory responses have not been fully identified. Intermediate-conductance Ca2+-activated K+ channels (IK) have been identified in biliary epithelium, but functional data are lacking. The aim of these studies therefore was to determine the location, function, and regulation of IK channels in biliary epithelial cells and to determine their potential contribution to ATP-stimulated secretion. Expression of IK-1 mRNA was found in both human Mz-Cha-1 biliary cells and polarized normal rat cholangiocyte (NRC) monolayers, and immunostaining revealed membrane localization with a predominant basolateral signal. In single Mz-Cha-1 cells, exposure to ATP activated K+ currents, increasing current density from 1.6 ± 0.1 to 7.6 ± 0.8 pA/pF. Currents were dependent on intracellular Ca2+ and sensitive to clotrimazole and TRAM-34 (specific IK channel inhibitors). Single-channel recording demonstrated that clotrimazole-sensitive K+ currents had a unitary conductance of 46.2 ± 1.5 pS, consistent with IK channels. In separate studies, 1-EBIO (an IK activator) stimulated K+ currents in single cells that were inhibited by clotrimazole. In polarized NRC monolayers, ATP significantly increased transepithelial secretion which was inhibited by clotrimazole. Lastly, ATP-stimulated K+ currents were inhibited by the P2Y receptor antagonist suramin and by the inositol 1,4,5-triphosphate (IP3) receptor inhibitor 2-APB. Together these studies demonstrate that IK channels are present in biliary epithelial cells and contribute to ATP-stimulated secretion through a P2Y-IP3 receptor pathway.

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21

Nakanuma, Yasuni, Goroku Ohta, Naoko Kono, Kenichi Kobayashi, and Yasuhiro Kato. "Electron microscopic observation of destruction of biliary epithelium in primary biliary cirrhosis." Liver 3, no. 4 (December 10, 2008): 238–48. http://dx.doi.org/10.1111/j.1600-0676.1983.tb00874.x.

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22

Rege, R. V., and E. W. Moore. "Convective movement of Ca2+ across guinea pig gallbladder epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 6 (June 1, 1992): G990—G995. http://dx.doi.org/10.1152/ajpgi.1992.262.6.g990.

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Recently, much interest has developed in biliary calcium because of its importance in the pathogenesis and composition of gallstones. While much progress has been made in understanding the thermodynamic factors that control biliary calcium concentrations, little is known about the kinetic factors that control the movement of calcium across the gallbladder epithelium. These studies measure guinea pig gallbladder epithelial permeability to Ca2+ during in vivo convective water movement across the membrane. Water movement, ranging from -15.2 (absorption) to 6.3 microliters.min-1.cm-2 (water entry), was induced by placing hypotonic, isotonic, and hypertonic solutions into the gallbladder lumen. Calcium movement was found to be directly and linearly related to water flow, indicating that Ca2+ moved with the convective water flow, presumably across paracellular channels. The slope of this relationship (0.602), representing the concentration of calcium in the fluid translocated across the gallbladder epithelium, was only about half that of plasma or luminal contents, indicating that calcium movement across the membrane was restricted. The mean sieving coefficient (1 - r) of guinea pig gallbladder, calculated from this slope, was approximately 0.5, indicating that the epithelium is only moderately permeable to Ca2+. The results suggest that intraluminal chelation of Ca2+ for the possible prevention and/or treatment of calcium-containing gallstones is a potentially feasible therapeutic modality.

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23

Fabris, Luca, Carlo Spirli, Massimiliano Cadamuro, Romina Fiorotto, and Mario Strazzabosco. "Emerging concepts in biliary repair and fibrosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 313, no. 2 (August 1, 2017): G102—G116. http://dx.doi.org/10.1152/ajpgi.00452.2016.

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Chronic diseases of the biliary tree (cholangiopathies) represent one of the major unmet needs in clinical hepatology and a significant knowledge gap in liver pathophysiology. The common theme in cholangiopathies is that the target of the disease is the biliary tree. After damage to the biliary epithelium, inflammatory changes stimulate a reparative response with proliferation of cholangiocytes and restoration of the biliary architecture, owing to the reactivation of a variety of morphogenetic signals. Chronic damage and inflammation will ultimately result in pathological repair with generation of biliary fibrosis and clinical progression of the disease. The hallmark of pathological biliary repair is the appearance of reactive ductular cells, a population of cholangiocyte-like epithelial cells of unclear and likely mixed origin that are able to orchestrate a complex process that involves a number of different cell types, under joint control of inflammatory and morphogenetic signals. Several questions remain open concerning the histogenesis of reactive ductular cells, their role in liver repair, their mechanism of activation, and the signals exchanged with the other cellular elements cooperating in the reparative process. This review contributes to the current debate by highlighting a number of new concepts derived from the study of the pathophysiology of chronic cholangiopathies, such as congenital hepatic fibrosis, biliary atresia, and Alagille syndrome.

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24

Fabris, L., M. Cadamuro, C. Spirlì, R. Fiorotto, A. Sonzogni, M. Colledan, S. Fagiuoli, L. Okolicsanyi, and M. Strazzabosco. "Evidence for epithelial–mesenchymal transition in the biliary epithelium of human cholangiocarcinoma." Digestive and Liver Disease 40, no. 5 (May 2008): A10—A11. http://dx.doi.org/10.1016/j.dld.2007.12.041.

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25

Perrone, R. D., S. A. Grubman, L. C. Rogers, D. W. Lee, E. Moy, S. L. Murray, V. E. Torres, and D. M. Jefferson. "Continuous epithelial cell lines from ADPKD liver cysts exhibit characteristics of intrahepatic biliary epithelium." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 3 (September 1, 1995): G335—G345. http://dx.doi.org/10.1152/ajpgi.1995.269.3.g335.

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We have produced continuous cell lines using retroviral transduction of SV40 large T antigen into epithelial cells removed from the lumen of liver cysts from four female patients with autosomal dominant polycystic kidney disease (ADPKD). Liver cyst-derived epithelial (LCDE) cell lines are grown in a hormonally supplemented medium in the presence of lethally irradiated NIH/3T3 fibroblast coculture. LCDE cells maintain their epithelial appearance and are positive for the biliary-specific markers cytokeratin 7 and 19 and gamma-glutamyl transpeptidase while being negative for hepatocyte markers. SV40 large T antigen is localized to the cell nucleus. LCDE cells have been grown continuously for periods exceeding 12 mo and 25 passages (170 population doublings). LCDE cells exhibit intracellular pH regulatory pathways that, with one exception, are similar to those found in normal intrahepatic biliary epithelium. These LCDE cell lines exhibit impaired alkalinization in response to Cl- substitution. This finding is suggestive of decreased function or abundance of a Cl-/HCO3- anion exchanger and could account for the failure of ADPKD hepatic cysts to secrete HCO3- in response to secretin.

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26

Freeman, Hugh J., and WC Peter Kwan. "Occult Celiac Disease Associated with Lymphocytic Sclerosing Cholangitis." Canadian Journal of Gastroenterology 8, no. 4 (1994): 249–52. http://dx.doi.org/10.1155/1994/597238.

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A 60-year-old male with dermatitis herpetiformis and a previously treated lymphoma involving an inguinal lymph node developed abnormal liver chemistry tests. Because of intermittent diarrhea, additional studies revealed lymphocytic colitis and occult celiac disease that responded to a gluten-free diet. A liver biopsy done to explore persistently abnormal liver chemistry tests showed a portal tract-centred inflammatory process characterized by biliary ductal proliferation, epithelial lymphocytosis and concentric lamellar fibrosis. Quantitation of immunoglobulins was normal and antimitochondrial antibodies were negative. Retrograde cholangiograms showed radiological features typical of primary sclerosing cholangius. The epithelial lymphocycosis reported in gastric, small and large intestinal mucosa of some patients with celiac disease may also be present in the biliary ductal columnar epithelium. This report provides additional evidence that celiac disease may be a far more extensive pathological process.

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27

Hayward, A. R., J. Levy, F. Facchetti, L. Notarangelo, H. D. Ochs, A. Etzioni, J. Y. Bonnefoy, M. Cosyns, and A. Weinberg. "Cholangiopathy and tumors of the pancreas, liver, and biliary tree in boys with X-linked immunodeficiency with hyper-IgM." Journal of Immunology 158, no. 2 (January 15, 1997): 977–83. http://dx.doi.org/10.4049/jimmunol.158.2.977.

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Abstract We report an association between X-linked immunodeficiency with hyper-IgM (XHIM) and carcinomas affecting the liver, pancreas, biliary tree, and associated neuroectodermal endocrine cells. The tumors were fatal in eight of nine cases and in most instances were preceded by chronic cholangiopathy and/or cirrhosis. An additional group of subjects with XHIM had chronic inflammation of the liver or bile ducts but no malignancy. Many patients with XHIM were infected with cryptosporidia. CD40 is normally expressed on regenerating or inflammed bile duct epithelium. A CD40+ hepatocellular carcinoma cell line, HepG2, susceptible to cryptosporidia and CMV infection became resistant when cell surface CD40 was cross-linked by a CD40 ligand fusion protein. Apoptosis was triggered in HepG2 cells if protein synthesis was blocked by cycloheximide or if the cells were infected by cryptosporidia. Ligation of CD40 on biliary epithelium may contribute to defense against infection by intracellular pathogens. We propose that the CD40 ligand mutations that cause XHIM deprive the biliary epithelium of one line of defense against intracellular pathogens and that malignant transformation in the biliary tree follows chronic infection or inflammation. The resulting tumors may then progress without check by an effective immune response. Patients with XHIM who have abnormal liver function tests should be considered at increased risk for cholangiopathy or malignancy.

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28

Vijayan, V., and CEL Tan. "A computer-generated three-dimensional view of the developing human biliary system." Proceedings, annual meeting, Electron Microscopy Society of America 54 (August 11, 1996): 626–27. http://dx.doi.org/10.1017/s0424820100165598.

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With the advent of computers, microscopy has entered an exciting new era of computerised three dimensional (3D) reconstruction. Using serial sections, it is now possible to generate complex 3D images, that can be rotated at various angles to study the organ systems of interest. In this project, the first of its kind, we have used computer generated 3D reconstruction to study the developing human biliary system.The human biliary system consists of the extra and intrahepatic components. The extrahepatic system develops from the embryonic hepatic diverticulum and is tubular from the start. The intrahepatic bile ducts arise from the Ductal Plate. The Ductal Plate comprises of sheets of biliary epithelium, with discontinuous luminal spaces, that appear within the mesenchyme along the portal vein branches. The Ductal Plate is remodelled into tubular definitive bile ducts by an orderly process of epithelial deletion and selection which occurs between 11-13 weeks of gestation

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29

Firrincieli, Delphine, Silvia Zuniga, Raoul Poupon, Chantal Housset, and Nicolas Chignard. "Role of Nuclear Receptors in the Biliary Epithelium." Digestive Diseases 29, no. 1 (2011): 52–57. http://dx.doi.org/10.1159/000324129.

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30

Kwon, Dong Hyang, Lynt B. Johnson, and Metin Ozdemirli. "Primary Epidermoid Cyst of Biliary Duct Presenting as Choledochal Cyst." International Journal of Surgical Pathology 25, no. 7 (May 16, 2017): 619–22. http://dx.doi.org/10.1177/1066896917710717.

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Choledochal cyst is a cystic dilation of the biliary tree that can increase the risk of malignancy in bile ducts and the gallbladder. These are usually lined by bile duct epithelium, which may undergo intestinal and squamous metaplasia. This is the first report of clinically diagnosed type II choledochal cyst that is entirely lined by metaplastic stratified squamous epithelium, unlike most other cysts, which are histologically lined by bile duct epithelium. This observation can potentially explain the underlying pathogenic mechanism of rare reports of squamous cell carcinomas arising in bile duct systems.

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31

Wilkie, J. S. Nimmo, J. A. Yager, P. N. Nation, E. G. Clark, H. G. G. Townsend, and J. D. Baird. "Chronic Eosinophilic Dermatitis: A Manifestation of a Multisystemic, Eosinophilic, Epitheliotropic Disease in Five Horses." Veterinary Pathology 22, no. 4 (July 1985): 297–305. http://dx.doi.org/10.1177/030098588502200401.

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A generalized, chronic, progressive, exfoliative dermatitis in five horses is described. Histologically, the lesion is characterized by a superficial and deep perivascular dermatitis which is eosinophil-rich with a marked lymphocytic and plasmacytic component, accompanied by marked acanthosis and hyperkeratosis. More severe cases progress to a lichenoid pattern with the same cellular composition with focal eosinophilic spongiosis and eosinophilic subcorneal pustules. Clinically, the disease is associated with chronic, severe weight loss and is fulminating. The skin lesions are accompanied by lymphoplasmacytic and eosinophilic infiltrates and formation of eosinophilic granulomas in other epithelial organs, most noticeably the pancreas, in which a chronic, fibrosing pancreatitis develops. Other epithelial organs involved to various degrees are salivary glands, the gastrointestinal system, including the oral cavity and esophagus, biliary epithelium and bronchial epithelium. The etiology of this disease is unknown.

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Harada, Kenichi, Yasunori Sato, Hiroko Ikeda, Maylee Hsu, Saya Igarashi, and Yasuni Nakanuma. "Notch1-Hes1 signalling axis in the tumourigenesis of biliary neuroendocrine tumours." Journal of Clinical Pathology 66, no. 5 (February 19, 2013): 386–91. http://dx.doi.org/10.1136/jclinpath-2012-201273.

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AimsBiliary neuroendocrine tumours (NETs) are rare and mostly exist as a component of mixed adenoneuroendocrine carcinomas (MANECs). Although the NET component in biliary MANECs is generally more malignant and clinically more important to the prognosis than the ordinary adenocarcinomatous component, the histogenesis of biliary NET has not been clarified. In this study, the role of the Notch1-Hes1 signalling axis in the histogenesis of biliary NETs was examined.MethodsImmunohistochemistry for Notch1, its ligand Jagged1 and Hes1 was performed using surgical specimens from 11 patients with biliary MANEC. Moreover, after the knock-down of Notch1 mRNA expression in a cholangiocarcinoma cell line, the expression of chromogranin A (a neuroendocrine marker) and Ascl1 (a neuroendocrine-inducing molecule inhibited by activated Hes1) was examined by quantitative PCR.ResultsHistological examination revealed that the adenocarcinomatous components were predominately located at the luminal surface of the MANEC and the majority of stromal invasion involved NET components. Ordinary adenocarcinomas and non-neoplastic biliary epithelium constantly expressed Notch1, Jagged1 and Hes1, but the expression of Notch1 and Hes1 was decreased or absent in NET components, suggesting interference with the Notch1-Hes1 signalling axis in biliary NET. Moreover, in the cholangiocarcinoma cell line in which the expression of Notch1 mRNA was knocked down, the mRNA expression of Ascl1 and chromogranin A was increased.ConclusionsThe Notch1-Hes1 signalling axis suppresses neuroendocrine differentiation and maintains tubular/acinar features in adenocarcinoma and non-neoplastic epithelium in the biliary tree. Moreover, a disruption of this signalling axis may be associated with the tumourigenesis of NETs in biliary MANEC.

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Rocha, Eduardo, Rogério A. F. Monteiro, and Carlos A. Pereira. "Presence of rodlet cells in the intrahepatic biliary ducts of the brown trout, Salmo trutta fario Linnaeus, 1758 (Teleostei, Salmonidae)." Canadian Journal of Zoology 72, no. 9 (September 1, 1994): 1683–87. http://dx.doi.org/10.1139/z94-225.

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We report for the first time rodlet cells in the epithelium of intrahepatic biliary ducts of the brown trout (Salmo trutta fario Linnaeus 1758). Such cells have not been described in the liver of any salmonid. Several developmental stages of the rodlet cells were found, including mature, discharging elements. The number of rodlet cells decreased from June to April. Intra-epithelial macrophages were found in close proximity to rodlet cells, suggesting a mild pathological reaction.

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Benson, Katherine K., Ankur Sheel, Shafia Rahman, Ashwini Esnakula, and Ashish Manne. "Understanding the Clinical Significance of MUC5AC in Biliary Tract Cancers." Cancers 15, no. 2 (January 9, 2023): 433. http://dx.doi.org/10.3390/cancers15020433.

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Biliary tract cancers (BTC) arise from biliary epithelium and include cholangiocarcinomas or CCA (including intrahepatic (ICC) and extrahepatic (ECC)) and gallbladder cancers (GBC). They often have poor outcomes owing to limited treatment options, advanced presentations, frequent recurrence, and poor response to available systemic therapy. Mucin 5AC (MUC5AC) is rarely expressed in normal biliary epithelium, but can be upregulated in tissues of benign biliary disease, premalignant conditions (e.g., biliary intraepithelial neoplasia), and BTCs. This mucin’s numerous glycoforms can be divided into less-glycosylated immature and heavily-glycosylated mature forms. Reported MUC5AC tissue expression in BTC varies widely, with some associations based on cancer location (e.g., perihilar vs. peripheral ICC). Study methods were variable regarding cancer subtypes, expression positivity thresholds, and MUC5AC glycoforms. MUC5AC can be detected in serum of BTC patients at high concentrations. The hesitancy in developing MUC5AC into a clinically useful biomarker in BTC management is due to variable evidence on the diagnostic and prognostic value. Concrete conclusions on tissue MUC5AC are difficult, but serum detection might be relevant for diagnosis and is associated with poor prognosis. Future studies are needed to further the understanding of the potential clinical value of MUC5AC in BTC, especially regarding predictive and therapeutic value.

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Merlen, Grégory, Nicolas Kahale, Jose Ursic-Bedoya, Valeska Bidault-Jourdainne, Hayat Simerabet, Isabelle Doignon, Zahra Tanfin, et al. "TGR5-dependent hepatoprotection through the regulation of biliary epithelium barrier function." Gut 69, no. 1 (February 5, 2019): 146–57. http://dx.doi.org/10.1136/gutjnl-2018-316975.

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ObjectiveWe explored the hypothesis that TGR5, the bile acid (BA) G-protein-coupled receptor highly expressed in biliary epithelial cells, protects the liver against BA overload through the regulation of biliary epithelium permeability.DesignExperiments were performed under basal and TGR5 agonist treatment. In vitro transepithelial electric resistance (TER) and FITC-dextran diffusion were measured in different cell lines. In vivo FITC-dextran was injected in the gallbladder (GB) lumen and traced in plasma. Tight junction proteins and TGR5-induced signalling were investigated in vitro and in vivo (wild-type [WT] and TGR5-KO livers and GB). WT and TGR5-KO mice were submitted to bile duct ligation or alpha-naphtylisothiocyanate intoxication under vehicle or TGR5 agonist treatment, and liver injury was studied.ResultsIn vitro TGR5 stimulation increased TER and reduced paracellular permeability for dextran. In vivo dextran diffusion after GB injection was increased in TGR5-knock-out (KO) as compared with WT mice and decreased on TGR5 stimulation. In TGR5-KO bile ducts and GB, junctional adhesion molecule A (JAM-A) was hypophosphorylated and selectively downregulated among TJP analysed. TGR5 stimulation induced JAM-A phosphorylation and stabilisation both in vitro and in vivo, associated with protein kinase C-ζ activation. TGR5 agonist-induced TER increase as well as JAM-A protein stabilisation was dependent on JAM-A Ser285 phosphorylation. TGR5 agonist-treated mice were protected from cholestasis-induced liver injury, and this protection was significantly impaired in JAM-A-KO mice.ConclusionThe BA receptor TGR5 regulates biliary epithelial barrier function in vitro and in vivo through an impact on JAM-A expression and phosphorylation, thereby protecting liver parenchyma against bile leakage.

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Hansel, Donna E., Anirban Maitra, John W. Lin, Michael Goggins, Pedram Argani, Charles J. Yeo, Steven Piantadosi, Steven D. Leach, and Andrew V. Biankin. "Expression of the Caudal-Type Homeodomain Transcription Factors CDX 1/2 and Outcome in Carcinomas of the Ampulla of Vater." Journal of Clinical Oncology 23, no. 9 (March 20, 2005): 1811–18. http://dx.doi.org/10.1200/jco.2005.03.068.

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Purpose Adenocarcinomas of the ampulla of Vater demonstrate a characteristic histology but vary significantly in outcome. As a consequence, prognostic factors for these cancers are poorly defined. The caudal-type homeodomain transcription factors 1 (CDX1) and 2 (CDX2) regulate axial development and intestinal differentiation. We assessed the expression of these putative intestinal epithelial-specific transcription factors and their influence on patient outcome. Patients and Methods Fifty-three resected carcinomas of the ampulla of Vater, 31 pancreatic ductal adenocarcinomas, and 15 extrahepatic biliary carcinomas were analyzed for CDX1 and CDX2 expression using immunohistochemistry. Results Forty percent of carcinomas of the ampulla of Vater but less than 5% of pancreatic and biliary adenocarcinomas expressed CDX. Expression of CDX was associated with a better prognosis (P = .0009). Individually, both CDX1 (P = .02) and CDX2 (P = .02) expression were associated with a survival advantage on univariate analysis. Advanced T stage (P = .02), lymph node metastases (P = .004), and vascular space invasion (P = .0009) were associated with a poor prognosis. Multivariate analysis revealed vascular space invasion (P = .01) and CDX expression (P = .01) to be independent prognostic factors. Conclusion Expression of CDX was an independent marker of outcome in patients with resected adenocarcinoma of the ampulla of Vater. Expression of CDX may distinguish good prognosis intestinal-like tumors, which potentially arise within intestinal epithelium, from poorer prognosis pancreatobiliary tumors, which arise in adjacent pancreatic and/or biliary ductal epithelium.

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Boyer, J. L. "Bile duct epithelium: frontiers in transport physiology." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 1 (January 1, 1996): G1—G5. http://dx.doi.org/10.1152/ajpgi.1996.270.1.g1.

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The bile duct epithelium is known to modify hepatic bile by both secretory and absorptive processes. However, identification and characterization of the transport systems that carry out these physiological functions at the cellular and molecular level have been slow compared with progress in understanding hepatic bile production. Recently, techniques have been developed that enable bile duct cells to be isolated in substantial number and purity and as intact polarized units that can be studied in vitro. These newer preparations have enabled classic physiological approaches to be performed directly with the bile duct epithelial tissues. Progress in this important area of biliary physiology is now rapid and forms the basis for this review.

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Vij, Mukul, and Mohamed Rela. "Biliary atresia: pathology, etiology and pathogenesis." Future Science OA 6, no. 5 (June 1, 2020): FSO466. http://dx.doi.org/10.2144/fsoa-2019-0153.

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Biliary atresia is a progressive fibrosing obstructive cholangiopathy of the intrahepatic and extrahepatic biliary system, resulting in obstruction of bile flow and neonatal jaundice. Histopathological findings in liver biopsies include the expansion of the portal tracts, with edematous fibroplasia and bile ductular proliferation, with bile plugs in duct lumen. Lobular morphological features may include variable multinucleate giant cells, bilirubinostasis and hemopoiesis. The etiopathogenesis of biliary atresia is multifactorial and multiple pathomechanisms have been proposed. Experimental and clinical studies have suggested that viral infection initiates biliary epithelium destruction and release of antigens that trigger a Th1 immune response, which leads to further injury of the bile duct, resulting in inflammation and obstructive scarring of the biliary tree. It has also been postulated that biliary atresia is caused by a defect in the normal remodelling process. Genetic predisposition has also been proposed as a factor for the development of biliary atresia.

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Zoltowska, Monika, Edgard E. Delvin, Khazal Paradis, Ernest Seidman, and Emile Levy. "Bile duct cells: a novel in vitro model for the study of lipid metabolism and bile acid production." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 2 (February 1, 1999): G407—G414. http://dx.doi.org/10.1152/ajpgi.1999.276.2.g407.

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Immortalized bile duct cells (BDC), derived from transgenic mice harboring the SV40 thermosensitive immortalizing mutant gene ts458, were utilized to investigate the role of the biliary epithelium in lipid and sterol metabolism. This cell model closely resembles the in vivo situation because it expresses the specific phenotypic marker cytokeratin 19 (CK-19), exhibits the formation of bile duct-like structures, and displays well-formed microvilli projected from the apical side to central lumen. The BDC were found to incorporate [14C]oleic acid (in nmol/mg protein) into triglycerides (121 ± 6), phospholipids (PL; 59 ± 3), and cholesteryl ester (16 ± 1). The medium lipid content represented 5.90 ± 0.16% ( P < 0.005) of the total intracellular production, indicating a limited lipid export capacity. Analysis of PL composition demonstrated the synthesis of all classes of polar lipids, with phosphatidylcholine and phosphatidylethanolamine accounting for 60 ± 1 and 24 ± 1%, respectively, of the total. Differences in PL distribution were apparent between cells and media. Substantial cholesterol synthesis was observed in BDC, as determined by the incorporation of [14C]acetate suggesting the presence of hydroxymethylglutaryl-CoA (HMG-CoA) reductase, the rate-limiting enzyme in the cholesterol biosynthetic pathway. With the use of [14C]acetate and [14C]cholesterol as precursors, both tauro- and glycoconjugates of bile acids were synthesized, indicating the presence of cholesterol 7α- and 26R-hydroxylases, the key enzymes involved in bile acid formation. The transport of bile acids was not limited, as shown by their marked accumulation in the medium (>6-fold of cell content). HMG-CoA reductase (53.0 ± 6.7), cholesterol 7α-hydroxylase (15.5 ± 0.5), and acyl-CoA:cholesterol acyltransferase (ACAT; 201.7 ± 10.2) activities (in pmol ⋅ min−1 ⋅ mg protein−1) were present in the microsomal fractions. Our data show that biliary epithelial cells actively synthesize lipids and may directly contribute bile acids to the biliary fluid in vivo. This BDC line thus represents an efficient experimental tool to evaluate biliary epithelium sterol metabolism and to study biliary physiology.

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Dubey, J. P., Kimberley J. Evason, and Zenta Walther. "Endogenous development of Cystoisospora belli in intestinal and biliary epithelium of humans." Parasitology 146, no. 07 (March 12, 2019): 865–72. http://dx.doi.org/10.1017/s003118201900012x.

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AbstractCystoisospora(Isospora)belliis a coccidian parasite of humans. It can cause serious digestive disorders involving infection of intestines, biliary tract and gallbladder, especially in those with depressed immunity. It has a direct fecal–oral transmission cycle. After ingestion of sporulated oocysts, the parasite multiplies asexually and sexually within host epithelial cells, resulting in unsporulated oocysts that are excreted in feces. The details of asexual and sexual stages are not known and certain inclusions in epithelial cells in biopsy samples have been erroneously identified recently asC. belli. Here, we provide details of developmental stages ofC. belliin two patients, in duodenal biopsy of one and biliary epithelium of the other. Immature and mature asexual stages (schizonts/meronts) were seen in epithelial cells. The merozoites were seen singly, in pairs and in groups in single parasitophorous vacuole (pv) in host cytoplasm. Immature and mature meronts were seen together in the same pv; up to eight nuclei were seen in meronts that retained elongated crescent shape; round multinucleated schizonts, seen in other coccidians, were not found. Meronts were up to 25µm long and contained up to ten merozoites that were 8–11µm long. The merozoites and meronts contained PAS-positive granules. Microgamonts (male) contained up to 30 nuclei that were arranged at the periphery and had condensed chromatin; 1–3 PAS-positive, eosinophilic, residual bodies were left when microgametes were formed. The microgametes were 4µm long and PAS-negative. All stages of macrogamonts, including oocysts were PAS-positive. The detailed description of the life cycle stages ofC. bellireported here should facilitate in histopathologic diagnosis of this parasite.

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Bründler, Marie-Anne, Norberto Rodriguez-Baez, Ron Jaffe, Arthur G. Weinberg, and Beverly Barton Rogers. "Adenovirus Ascending Cholangiohepatitis." Pediatric and Developmental Pathology 6, no. 2 (March 2003): 156–59. http://dx.doi.org/10.1007/s10024-002-0063-4.

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Three children, two with liver transplants and one with acquired human immunodeficiency virus (HIV) infection, presented with hepatitis accompanied by elevated gamma glutamyl transpeptidase. Biopsies revealed cholangiohepatitis caused by adenovirus infection. There was a progressive loss of interlobular bile ducts in two of the patients. In one patient, infection of the biliary tree was marked by a necrotizing cholangitis, with adenoviral inclusions noted in the biliary epithelium. In each patient, there was evidence of adenovirus gastrointestinal infection. This is the first report of adenoviral infection of the biliary tree in humans. It is hypothesized that adenovirus cholangiohepatitis occurs as a result of ascending infection from the gastrointestinal tract to the biliary tree.

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Alvaro, Domenico, Gianfranco Alpini, Paolo Onori, Lucia Perego, Gianluca Svegliati Baroni, Antonio Franchitto, Leonardo Baiocchi, et al. "Estrogens stimulate proliferation of intrahepatic biliary epithelium in rats." Gastroenterology 119, no. 6 (December 2000): 1681–91. http://dx.doi.org/10.1053/gast.2000.20184.

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Savard, Christopher E., Phillip Watts, and Sum P. Lee. "Lipopolysaccharide stimulation of TNFA secretion by human biliary epithelium." Gastroenterology 118, no. 4 (April 2000): A3. http://dx.doi.org/10.1016/s0016-5085(00)82077-6.

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Alvaro, D., L. Marucci, A. Gigliozzi, G. Alpini, E. Papa, M. Delle Monache, R. Monterubbianesi, L. Capocaccia, and A. Benedetti. "Corticosteroids modulate the secretory processes of intrahepatic biliary epithelium." Journal of Hepatology 32 (2000): 118. http://dx.doi.org/10.1016/s0168-8278(00)80785-0.

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Mancinelli, Romina, Francesca Olivero, Guido Carpino, Diletta Overi, Luigi Rosa, Maria Stefania Lepanto, Antimo Cutone, et al. "Role of lactoferrin and its receptors on biliary epithelium." BioMetals 31, no. 3 (March 17, 2018): 369–79. http://dx.doi.org/10.1007/s10534-018-0094-6.

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Eberhard, D., D. Tosh, and J. M. W. Slack. "Origin of pancreatic endocrine cells from biliary duct epithelium." Cellular and Molecular Life Sciences 65, no. 21 (September 22, 2008): 3467–80. http://dx.doi.org/10.1007/s00018-008-8427-1.

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Dutta, Amal K., Kangmee Woo, Al-karim Khimji, Charles Kresge, and Andrew P. Feranchak. "Mechanosensitive Cl− secretion in biliary epithelium mediated through TMEM16A." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 1 (January 1, 2013): G87—G98. http://dx.doi.org/10.1152/ajpgi.00154.2012.

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Bile formation by the liver is initiated by canalicular transport at the hepatocyte membrane, leading to an increase in ductular bile flow. Thus, bile duct epithelial cells (cholangiocytes), which contribute to the volume and dilution of bile through regulated Cl− transport, are exposed to changes in flow and shear force at the apical membrane. The aim of the present study was to determine if fluid flow, or shear stress, is a signal regulating cholangiocyte transport. The results demonstrate that, in human and mouse biliary cells, fluid flow, or shear, increases Cl− currents and identify TMEM16A, a Ca2+-activated Cl− channel, as the operative channel. Furthermore, activation of TMEM16A by flow is dependent on PKCα through a process involving extracellular ATP, binding purinergic P2 receptors, and increases in intracellular Ca2+ concentration. These studies represent the initial characterization of mechanosensitive Cl− currents mediated by TMEM16A. Identification of this novel mechanosensitive secretory pathway provides new insight into bile formation and suggests new therapeutic targets to enhance bile formation in the treatment of cholestatic liver disorders.

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Balabaud, C., P. Bioulac-Sage, L. Boussarie, and C. Bedin. "Hypertrophy of biliary epithelium in rats with portacaval shunt." Liver 3, no. 6 (December 10, 2008): 409–12. http://dx.doi.org/10.1111/j.1600-0676.1983.tb00896.x.

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Hossain, Moazzem, Osamu Murahashi, Hisami Ando, Kentiro Kaneko, and Takahiro Ito. "Proliferation of intrahepatic bile-duct epithelium in biliary atresia." Pediatric Surgery International 11, no. 2-3 (March 1996): 126–29. http://dx.doi.org/10.1007/bf00183743.

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Ehrlich, Laurent, Marinda Scrushy, Fanyin Meng, Terry C. Lairmore, Gianfranco Alpini, and Shannon Glaser. "Biliary epithelium: A neuroendocrine compartment in cholestatic liver disease." Clinics and Research in Hepatology and Gastroenterology 42, no. 4 (September 2018): 296–305. http://dx.doi.org/10.1016/j.clinre.2018.03.009.

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