Initiation of acute pancreatitis by heparan sulphate in the rat.
(2008) In Scandinavian Journal of Gastroenterology 43(4). p.480-489- Abstract
- OBJECTIVE: The initiating events in the onset of pancreatitis are poorly understood. Possible candidates may be endogenous ligands, acting on receptors within ductal, acinar or stellate cells, which have previously been shown to cause a systemic inflammatory response syndrome. The aim of this study was to investigate whether acute pancreatitis could be induced by heparan sulphate (HS)infused into the pancreatic ducts in the rat. MATERIAL AND METHODS: Retrograde biliary-pancreatic infusion of heparan sulphate of different structures, taurodeoxycholate (TDC) or phosphate buffered saline (PBS) was performed. Local pancreatic inflammation was evaluated after 6 h by means of morphological evaluation, neutrophil and macrophage infiltration and... (More)
- OBJECTIVE: The initiating events in the onset of pancreatitis are poorly understood. Possible candidates may be endogenous ligands, acting on receptors within ductal, acinar or stellate cells, which have previously been shown to cause a systemic inflammatory response syndrome. The aim of this study was to investigate whether acute pancreatitis could be induced by heparan sulphate (HS)infused into the pancreatic ducts in the rat. MATERIAL AND METHODS: Retrograde biliary-pancreatic infusion of heparan sulphate of different structures, taurodeoxycholate (TDC) or phosphate buffered saline (PBS) was performed. Local pancreatic inflammation was evaluated after 6 h by means of morphological evaluation, neutrophil and macrophage infiltration and levels of plasma amylase. Systemic inflammation was evaluated by measuring plasma IL-6, MCP-1 and CINC-1 concentrations. RESULTS: Heparan sulphate induced a local inflammatory response visualized as a rapid infiltration of neutrophils and macrophages into the pancreas. Heparan sulphate induced inflammation and oedema without causing damage to acinar cells, as measured by morphological changes and plasma amylase concentrations. Furthermore, an increase in serum concentrations of CINC-1 and IL-6 was seen. The positive control (TDC) had increased levels of all variables analysed and the negative control (heparan sulphate administered intraperitoneally) was without effects. CONCLUSIONS: Our findings suggest a receptor-mediated innate immune response of the pancreatic cells induced by heparan sulphate. This finding may be helpful in elucidating some of the mechanisms involved during the initiation of pancreatitis, as well as in the search for a potential future therapeutic application. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1052157
- author
- Axelsson, Jakob B LU ; Norrman, Gustav ; Malmström, Anders LU ; Weström, Björn LU and Andersson, Roland LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scandinavian Journal of Gastroenterology
- volume
- 43
- issue
- 4
- pages
- 480 - 489
- publisher
- Taylor & Francis
- external identifiers
-
- pmid:18365914
- wos:000254347500013
- scopus:41349084212
- pmid:18365914
- ISSN
- 1502-7708
- DOI
- 10.1080/00365520701733814
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Matrix biology (013212025), Surgery (Lund) (013009000), Functional Zoology (432112239), Cell and Matrix Biology (LUR000002)
- id
- de7cb655-c19e-4c31-b36f-681304070868 (old id 1052157)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/18365914?dopt=Abstract
- date added to LUP
- 2016-04-04 09:16:03
- date last changed
- 2022-03-15 18:31:23
@article{de7cb655-c19e-4c31-b36f-681304070868, abstract = {{OBJECTIVE: The initiating events in the onset of pancreatitis are poorly understood. Possible candidates may be endogenous ligands, acting on receptors within ductal, acinar or stellate cells, which have previously been shown to cause a systemic inflammatory response syndrome. The aim of this study was to investigate whether acute pancreatitis could be induced by heparan sulphate (HS)infused into the pancreatic ducts in the rat. MATERIAL AND METHODS: Retrograde biliary-pancreatic infusion of heparan sulphate of different structures, taurodeoxycholate (TDC) or phosphate buffered saline (PBS) was performed. Local pancreatic inflammation was evaluated after 6 h by means of morphological evaluation, neutrophil and macrophage infiltration and levels of plasma amylase. Systemic inflammation was evaluated by measuring plasma IL-6, MCP-1 and CINC-1 concentrations. RESULTS: Heparan sulphate induced a local inflammatory response visualized as a rapid infiltration of neutrophils and macrophages into the pancreas. Heparan sulphate induced inflammation and oedema without causing damage to acinar cells, as measured by morphological changes and plasma amylase concentrations. Furthermore, an increase in serum concentrations of CINC-1 and IL-6 was seen. The positive control (TDC) had increased levels of all variables analysed and the negative control (heparan sulphate administered intraperitoneally) was without effects. CONCLUSIONS: Our findings suggest a receptor-mediated innate immune response of the pancreatic cells induced by heparan sulphate. This finding may be helpful in elucidating some of the mechanisms involved during the initiation of pancreatitis, as well as in the search for a potential future therapeutic application.}}, author = {{Axelsson, Jakob B and Norrman, Gustav and Malmström, Anders and Weström, Björn and Andersson, Roland}}, issn = {{1502-7708}}, language = {{eng}}, number = {{4}}, pages = {{480--489}}, publisher = {{Taylor & Francis}}, series = {{Scandinavian Journal of Gastroenterology}}, title = {{Initiation of acute pancreatitis by heparan sulphate in the rat.}}, url = {{http://dx.doi.org/10.1080/00365520701733814}}, doi = {{10.1080/00365520701733814}}, volume = {{43}}, year = {{2008}}, }