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Initiation of acute pancreatitis by heparan sulphate in the rat.

Axelsson, Jakob B LU ; Norrman, Gustav; Malmström, Anders LU ; Weström, Björn LU and Andersson, Roland LU (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)
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author
organization
publishing date
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
ISSN
1502-7708
DOI
10.1080/00365520701733814
language
English
LU publication?
yes
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
2008-04-01 08:56:29
date last changed
2017-01-01 07:45:41
@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},
  volume       = {43},
  year         = {2008},
}