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Har-Zahav, A.

Publications and source records attributed to Har-Zahav, A..

2 recordsLinked to original sources

Human Vascularized Bile Duct-on-a Chip: A multi-cellular micro-physiological system for studying Primary Sclerosing Cholangitis

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease in which the bile ducts of the liver become inflamed and scarred. Scarred bile ducts eventually narrow and obstruct and can cause additional liver pathology including liver failure, repeated infections, and tumors. The pathogenesis of PSC remains largely unknown, partly due to difficulty in obtaining cholangiocytes and partly due to a paucity of in vitro models that capture the various factors contributing to disease progression. Here we report the development of a human vascularized bile duct-on-a-chip that models blood vessels and bile ducts structurally and functionally in three dimensions and includes cholangiocytes derived from control and PSC patient tissue and bile. The flow of blood and bile was modeled by perfusion of cell-lined channels, and cholangiocytes and endothelial cells displayed differential responses to perfusion. Normal and PSC cholangiocytes polarized normally, formed mature tight junctions and displayed similar permeability, comparable to ex vivo measurements. The model with PSC cholangiocytes, however, became more inflammatory than the normal under the stimulation of IL-17A, which induced PBMC and differentiated Th17 cells in the vascular channel to transmigrate more through the endothelial layer of the vascular compartment. In sum, this human vascularized bile duct-on-a-chip recapitulated the vascular-biliary interface structurally and functionally and represents a novel multicellular platform to study inflammatory and fibrotic cholangiopathies such as PSC.

bioengineering↗

Periductal bile acid exposure causes cholangiocyte injury and fibrosis

IntroductionBile duct integrity is essential for the maintenance of the structure and function of the biliary tree. We previously showed that cholangiocyte injury in a toxic model of biliary atresia leads to increased monolayer permeability. Increased epithelial permeability was also shown in other cholangiopathies. We hypothesized that after initial cholangiocyte injury, leakage of bile acids into the duct submucosa propagates cholangiocyte damage and fibrosis. We thus aimed to determine the impact of bile acid exposure on cholangiocytes and the potential therapeutic effect of a non-toxic bile acid. Materials and methodsExtrahepatic bile duct explants were isolated from adult and neonatal BALB/c mice. Explants were cultured with or without glycochenodeoxycholic acid and ursodeoxycholic acid. They were then fixed and stained. ResultsExplants treated with glycochenodeoxycholic acid demonstrated cholangiocyte injury with monolayer disruption and partial lumen obstruction compared to control ducts. Massons trichrome stains revealed increased collagen fibers. Myofibroblast marker -SMA stains were significantly elevated in the periductal region. The addition of ursodeoxycholic acid resulted in decreased cholangiocyte injury and reduced fibrosis. ConclusionsBile acid leakage into the submucosa after initial cholangiocyte injury may serve as a possible mechanism of disease propagation and progressive fibrosis in cholangiopathies.

physiology↗