Fatty acid ethyl ester (FAEE) associated acute pancreatitis: An ex-vivo study using human pancreatic acini.


Journal

Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
ISSN: 1424-3911
Titre abrégé: Pancreatology
Pays: Switzerland
ID NLM: 100966936

Informations de publication

Date de publication:
Dec 2020
Historique:
received: 06 05 2020
revised: 09 09 2020
accepted: 08 10 2020
pubmed: 21 10 2020
medline: 6 10 2021
entrez: 20 10 2020
Statut: ppublish

Résumé

Fatty acid ethyl esters (FAEEs), are produced by non-oxidative alcohol metabolism and can cause acinar cell damage and subsequent acute pancreatitis in rodent models. Even though experimental studies have elucidated the FAEE mediated early intra-acinar events, these mechanisms have not been well studied in humans. In the present study, we evaluate the early intra-acinar events and inflammatory response in human pancreatic acinar tissues and cells in an ex-vivo model. Experiments were conducted using normal human pancreatic tissues exposed to FAEE. Subcellular fractionation was performed on tissue homogenates and trypsin and cathepsin B activities were estimated in these fractions. Acinar cell injury was evaluated by histology and immunohistochemistry. Cytokine release from exposed acinar cells was evaluated by performing Immuno-fluorescence. Serum was collected from patients with AP within the first 72 h of symptom onset for cytokine estimation using FACS. We observed significant trypsin activation and acinar cell injury in FAEE treated tissue. Cathepsin B was redistributed from lysosomal to zymogen compartment at 30 min of FAEE exposure. IHC results indicated the presence of apoptosis in pancreatic tissue at 1 & 2hrs of FAEE exposure. We also observed a time dependent increase in secretion of cytokines IL-6, IL-8, TNF-α from FAEE treated acinar tissue. There was also a significant elevation in plasma cytokines in patents with alcohol associated AP within 72 h of symptom onset. Our data suggest that alcohol metabolites can cause acute acinar cell damage and subsequent cytokine release which could eventually culminant in SIRS.

Sections du résumé

BACKGROUND & AIM OBJECTIVE
Fatty acid ethyl esters (FAEEs), are produced by non-oxidative alcohol metabolism and can cause acinar cell damage and subsequent acute pancreatitis in rodent models. Even though experimental studies have elucidated the FAEE mediated early intra-acinar events, these mechanisms have not been well studied in humans. In the present study, we evaluate the early intra-acinar events and inflammatory response in human pancreatic acinar tissues and cells in an ex-vivo model.
METHODS METHODS
Experiments were conducted using normal human pancreatic tissues exposed to FAEE. Subcellular fractionation was performed on tissue homogenates and trypsin and cathepsin B activities were estimated in these fractions. Acinar cell injury was evaluated by histology and immunohistochemistry. Cytokine release from exposed acinar cells was evaluated by performing Immuno-fluorescence. Serum was collected from patients with AP within the first 72 h of symptom onset for cytokine estimation using FACS.
RESULTS RESULTS
We observed significant trypsin activation and acinar cell injury in FAEE treated tissue. Cathepsin B was redistributed from lysosomal to zymogen compartment at 30 min of FAEE exposure. IHC results indicated the presence of apoptosis in pancreatic tissue at 1 & 2hrs of FAEE exposure. We also observed a time dependent increase in secretion of cytokines IL-6, IL-8, TNF-α from FAEE treated acinar tissue. There was also a significant elevation in plasma cytokines in patents with alcohol associated AP within 72 h of symptom onset.
CONCLUSION CONCLUSIONS
Our data suggest that alcohol metabolites can cause acute acinar cell damage and subsequent cytokine release which could eventually culminant in SIRS.

Identifiants

pubmed: 33077383
pii: S1424-3903(20)30778-X
doi: 10.1016/j.pan.2020.10.027
pii:
doi:

Substances chimiques

Esters 0
Fatty Acids 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1620-1630

Informations de copyright

Copyright © 2020. Published by Elsevier B.V.

Auteurs

Aparna Jakkampudi (A)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India.

Ramaiah Jangala (R)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India.

Ratnakar Reddy (R)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India.

Balkumar Reddy (B)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India.

G Venkat Rao (G)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India; Dept. of Surgical Gastroenterology, Asian Institute of Gastroenterology, India.

Rebala Pradeep (R)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India; Dept. of Surgical Gastroenterology, Asian Institute of Gastroenterology, India.

D Nageshwar Reddy (D)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India; Dept. of Medical Gastroenterology, Asian Institute of Gastroenterology, India.

Rupjyoti Talukdar (R)

Wellcome-DBT India Alliance Labs., Institute of Basic and Translational Research, Asian Healthcare Foundation, India; Dept. of Medical Gastroenterology, Asian Institute of Gastroenterology, India. Electronic address: rup_talukdar@yahoo.com.

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