The Biliary HCO3 − Umbrella: A Unifying Hypothesis on Pathogenetic and Therapeutic Aspects of Fibrosing Cholangiopathies
Open accessAbstract
This review focuses on the hypothesis that biliary HCO Symbol secretion in humans serves to maintain an alkaline pH near the apical surface of hepatocytes and cholangiocytes to prevent the uncontrolled membrane permeation of protonated glycine-conjugated bile acids. Functional impairment of this biliary HCO Symbol umbrella or its regulation may lead to enhanced vulnerability of cholangiocytes and periportal hepatocytes toward the attack of apolar hydrophobic bile acids. An intact interplay of hepatocellular and cholangiocellular adenosine triphosphate (ATP) secretion, ATP/P2Y- and bile salt/TGR5-mediated Cl−/ HCO Symbol exchange and HCO Symbol secretion, and alkaline phosphatase–mediated ATP breakdown may guarantee a stable biliary HCO Symbol umbrella under physiological conditions. Genetic and acquired functional defects leading to destabilization of the biliary HCO Symbol umbrella may contribute to development and progression of various forms of fibrosing/sclerosing cholangitis. (Hepatology 2010)
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AE2 and an intact biliary glycocalyx help maintain a protective biliary umbrella against hydrophobic bile acid monomers.
“the Cl À /HCO 3 À exchanger (AE2; anion exchanger 2) and an intact biliary glycocalyx are important in maintaining a protective biliary 'umbrella' against invasion of hydrophobic bile acid monomers.”
From EASL Clinical Practice Guidelines: The diagnosis and management of patients with primary biliary cholangitis. (2017) · cites this paper as [27]
In “Cholangiocyte Survival Strategy: The Biliary HCO₃⁻ Umbrella” (page not provided), the paper identifies AE2 as responsible for most biliary bicarbonate secretion and proposes that the resulting umbrella protects against hydrophobic bile acid monomers. The Fig. 2 caption says the biliary glycocalyx *might* contribute to local pH regulation; it does not establish that an intact glycocalyx is important for maintaining the umbrella. The citing sentence states that speculative contribution more firmly than the source does. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn PBC, downregulation of AE2 can sensitise cholangiocytes to apoptotic insults by activating adenylyl cyclase.
“In patients with PBC, downregulation of AE2 can sensitize cholangiocytes to apoptotic insults by activating adenylyl cyclase.”
From EASL Clinical Practice Guidelines: The diagnosis and management of patients with primary biliary cholangitis. (2017) · cites this paper as [27]
The Summary and Outlook (page unavailable) links AE2 impairment in PBC to greater cholangiocyte vulnerability to bile-acid damage. The paper also discusses apoptosis as a possible consequence of bile-acid injury, but it does not say that AE2 downregulation sensitizes cells to apoptotic insults by activating adenylyl cyclase. (LLM, conf=0.86)
Experimental — accuracy not yet measuredHydrophobic bile acids such as glycochenodeoxycholic acid suppress AE2 expression in biliary epithelial cells by inducing reactive oxygen species and cell senescence, leading to bile duct inflammation.
“hydrophobic bile acids (glycochenodeoxycholic acid) suppress AE2 expression in biliary epithelial cells by inducing reactive oxygen species and biliary epithelial cell senescence, leading to bile duct inflammation”
From EASL Clinical Practice Guidelines: The diagnosis and management of patients with primary biliary cholangitis. (2017) · cites this paper as [27]
The “Biliary HCO₃⁻” section describes glycochenodeoxycholate causing injury in mouse gastric mucosa at low pH, and bile acids causing oxidative stress in human esophageal cells. It also discusses bile-salt injury to cholangiocytes, but does not say that glycochenodeoxycholic acid suppresses cholangiocyte AE2 expression through reactive oxygen species or senescence, or establish the claimed chain leading to bile duct inflammation. Page numbers were not available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredSenescent and apoptotic biliary epithelial cells secrete mediators that activate hepatic stellate cells, perpetuate inflammation, and promote fibrosis and biliary stasis.
“Both senescent and apoptotic cells secrete mediators that activate hepatic stellate cells (although PPARc and PPARd ligation may reduce this activation), perpetuate inflammation, and promote fibrosis and further biliary stasis.”
From EASL Clinical Practice Guidelines: The diagnosis and management of patients with primary biliary cholangitis. (2017) · cites this paper as [27]
The Biliary HCO₃ section (page unavailable) says cholangiocytes may undergo apoptosis, while the TGR5 section (page unavailable) says cholangiocytes release ATP and extracellular ATP can increase an inflammatory cytokine and recruit macrophages. The paper does not link mediator release specifically to senescent or apoptotic cells, or describe the claimed activation of hepatic stellate cells and resulting fibrosis and further biliary stasis. (LLM, conf=0.78)
Experimental — accuracy not yet measuredIn PBC, impaired apical AE2 activity and bicarbonate secretion cause unchaperoned bile acids to interfere with the biliary epithelial cell membrane, making cells vulnerable to pro-senescent and pro-apoptotic effects; unchaperoned bile acids further inhibit AE activity, weaken the bicarbonate umbrella, induce immune-response molecules, and promote apoptosis.
“In PBC, impaired activity of the apical AE2 and bicarbonate secretion lead to unchaperoned BA directly interfering with the BEC membrane.BEC are then vulnerable to the pro-senescent and pro-apoptotic effects of BA; unchaperoned BA further inhibit the activity of AE.This further weakens the bicarbonate umbrella, induces the expression of molecules that promote the immune response (CD40, HLA-DR and”
From EASL Clinical Practice Guidelines: The diagnosis and management of patients with primary biliary cholangitis. (2017) · cites this paper as [27]
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Self-citationNevens, F., Trauner, M. A., & Manns, M. P. (2022) · Journal of Hepatology · doi:10.1016/j.jhep.2022.10.007 · Cited by 51 · see citing works
- Authors
- Beuers, U., Hohenester, S., de Buy Wenniger, L. J. M., Kremer, A. E., Jansen, P. L. M., & Elferink, R. P. J. O.
- Affiliations
- Amsterdam UMC Location University of Amsterdam (NL)
- Corresponding author
- Beuers, Ulrich
- Venue
- Hepatology
- Published
- 2010-10
- Volume
- 52
- Issue
- 4
- Pages
- 1489-1496
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2063118624
- Semantic Scholar
- ac7bf18f0d355679c143ca5cb16178853655540a
- Cited by
- 351
- References
- 65
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 20 · 2023: 24 · 2022: 26 · 2021: 25 · 2020: 25 · 2019: 25 · 2018: 24 · 2017: 34 · 2016: 16 · 2015: 30 · 2014: 16 · 2013: 18 · 2012: 20
- FWCI
- 2.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (submittedVersion)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Health Sciences › Medicine › Surgery › Pediatric Hepatobiliary Diseases and Treatments
- Keywords
- sclerosing cholangitis, bile acid toxicity, glycine-conjugated bile acids, cholangiocytes, hepatocytes, ATP release, P2Y receptors, TGR5, chloride/bicarbonate exchange, alkaline phosphatase, bile acid metabolism, pathogenesis
- MeSH terms
- Adenosine Triphosphate, Animals, Bicarbonates, Bile Acids and Salts, Bile Ducts, Humans, Hydrogen-Ion Concentration, Micelles, Phospholipids, Cholangitis, Sclerosing, Receptors, Purinergic P2, Chloride-Bicarbonate Antiporters
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