Antimicrobial glycoprotein 2 (GP2) in gallstones, bile fluid and peribiliary glands of patients with primary sclerosing cholangitis.

Bile ducts Cholangitis Cholelithiasis Peribiliary gland Zymogen granule membrane glycoprotein

Journal

Clinica chimica acta; international journal of clinical chemistry
ISSN: 1873-3492
Titre abrégé: Clin Chim Acta
Pays: Netherlands
ID NLM: 1302422

Informations de publication

Date de publication:
02 Jul 2024
Historique:
received: 26 09 2023
revised: 28 05 2024
accepted: 28 06 2024
medline: 5 7 2024
pubmed: 5 7 2024
entrez: 4 7 2024
Statut: aheadofprint

Résumé

Glycoprotein-2 (GP2) IgA is a predictor of disease severity in primary sclerosing cholangitis (PSC). We examined GP2's occurrence in the biliary tract, the site of inflammation. GP2 was analyzed using ELISA, immunoblotting, mass spectrometry, and immunohistochemistry. The samples included: 20 bile and 30 serum samples from PSC patients, 23 bile and 11 serum samples from patients with gallstone disease (GD), 15 bile samples from healthy individuals undergoing liver-donation surgery (HILD), 20 extracts of gallstones (GE) obtained during cholecystectomy, and 101 blood-donor sera. Biliary GP2 concentrations were significantly higher in patients with PSC and GD than in HILD (p < 0.0001). Serum GP2 levels were similar in PSC, and GD patients and controls, but lower than in bile (p < 0.0001). GP2 was detected in all 20 GEs. Mass spectrometry identified GP2 in the bile of 2 randomly selected GD and 2 PSC patients, and in none of 2 HILD samples. GP2 was found in peribiliary glands in 8 out of 12 PSC patients, showing morphological changes in acinar cells, but not in GD-gallbladders. GP2 is present in bile of PSC and GD patients. It is synthesized in the peribiliary glands of PSC patients, supporting a pathogenic role for biliary GP2 in PSC.

Sections du résumé

BACKGROUND BACKGROUND
Glycoprotein-2 (GP2) IgA is a predictor of disease severity in primary sclerosing cholangitis (PSC). We examined GP2's occurrence in the biliary tract, the site of inflammation.
METHODS METHODS
GP2 was analyzed using ELISA, immunoblotting, mass spectrometry, and immunohistochemistry. The samples included: 20 bile and 30 serum samples from PSC patients, 23 bile and 11 serum samples from patients with gallstone disease (GD), 15 bile samples from healthy individuals undergoing liver-donation surgery (HILD), 20 extracts of gallstones (GE) obtained during cholecystectomy, and 101 blood-donor sera.
RESULTS RESULTS
Biliary GP2 concentrations were significantly higher in patients with PSC and GD than in HILD (p < 0.0001). Serum GP2 levels were similar in PSC, and GD patients and controls, but lower than in bile (p < 0.0001). GP2 was detected in all 20 GEs. Mass spectrometry identified GP2 in the bile of 2 randomly selected GD and 2 PSC patients, and in none of 2 HILD samples. GP2 was found in peribiliary glands in 8 out of 12 PSC patients, showing morphological changes in acinar cells, but not in GD-gallbladders.
CONCLUSIONS CONCLUSIONS
GP2 is present in bile of PSC and GD patients. It is synthesized in the peribiliary glands of PSC patients, supporting a pathogenic role for biliary GP2 in PSC.

Identifiants

pubmed: 38964568
pii: S0009-8981(24)02093-X
doi: 10.1016/j.cca.2024.119841
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

119841

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Steffi Lopens (S)

Institute of Biotechnology, Faculty of Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany; Medipan GmbH, Dahlewitz, Germany.

Peter Schierack (P)

Institute of Biotechnology, Faculty of Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany; Faculty of Health Sciences Brandenburg, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany.

Jenny Krause (J)

Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Michał Piaszczyński (M)

Department of General, Vascular and Transplant Surgery, Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, Poland.

Robert Król (R)

Department of General, Vascular and Transplant Surgery, Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, Poland.

Robert Staroń (R)

Department of Gastroenterology and Hepatology with Internal Disease Unit, Teaching Hospital No 1 in Rzeszów, Rzeszów, Poland; Medical Department, University of Rzeszów, Rzeszów, Poland.

Łukasz Krupa (Ł)

Department of Gastroenterology and Hepatology with Internal Disease Unit, Teaching Hospital No 1 in Rzeszów, Rzeszów, Poland; Medical Department, University of Rzeszów, Rzeszów, Poland.

Krzysztof Gutkowski (K)

Department of Gastroenterology and Hepatology with Internal Disease Unit, Teaching Hospital No 1 in Rzeszów, Rzeszów, Poland; Medical Department, University of Rzeszów, Rzeszów, Poland.

Beata Kruk (B)

Laboratory of Metabolic Liver Diseases, Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.

Michał Grąt (M)

Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.

Marek Krawczyk (M)

Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.

Waldemar Patkowski (W)

Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.

Fabian Glaser (F)

Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Stefan Rödiger (S)

Institute of Biotechnology, Faculty of Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany; Faculty of Health Sciences Brandenburg, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany.

Kai Grossmann (K)

GA Generic Assays GmbH, Senftenberg, Germany.

Jacek Pająk (J)

Department of Pathomorphology and Molecular Diagnostics, Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, Poland.

Piotr Milkiewicz (P)

Liver and Internal Medicine Unit, Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Warsaw, Poland; Translational Medicine Group, Pomeranian Medical University, Szczecin, Poland.

Frank Lammert (F)

Department of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany.

Krzysztof Zieniewicz (K)

Laboratory of Metabolic Liver Diseases, Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.

Christoph Schramm (C)

Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Dirk Roggenbuck (D)

Institute of Biotechnology, Faculty of Environment and Natural Sciences, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany; Faculty of Health Sciences Brandenburg, Brandenburg University of Technology Cottbus-Senftenberg, Senftenberg, Germany. Electronic address: dirk.roggenbuck@b-tu.de.

Marcin Krawczyk (M)

Laboratory of Metabolic Liver Diseases, Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland; Department of Medicine II, Saarland University Medical Center, Saarland University, Homburg, Germany.

Classifications MeSH