Proposed protective mechanism of the pancreas in the rat

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Axelsson, Jakob BLund University,Lunds universitet,Matrixbiologi,Forskargrupper vid Lunds universitet,Kirurgi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Matrix Biology,Lund University Research Groups,Surgery (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine (author)

Proposed protective mechanism of the pancreas in the rat

Article/chapterEnglish2010

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Springer Science and Business Media LLC,2010

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LIBRIS-ID:oai:lup.lub.lu.se:d58e17a3-52ea-4fba-9591-740a29cbf50e
https://lup.lub.lu.se/record/1629081URI
https://doi.org/10.1186/1476-9255-7-24DOI

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Language:English
Summary in:English

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Background: Heparan sulphate is known to have various functions in the animal body, including surveillance of tissue integrity. Administered intraperitoneally, it induces a systemic inflammatory response syndrome and when given locally in the pancreas it initiates a protective inflammatory response. The aim of the present study was to investigate the underlying mechanisms behind cell recruitment following intra-ductal infusion of heparan sulphate. Methods: Rats were subjected to intraductal-infusion of heparan sulphate, lipopolysaccharide and phosphate buffered saline into the pancreas. Pancreatic tissue was harvested 1, 3, 6, 9 or 48 hours after infusion and stained immunohistochemically for myeloperoxidase, ED-1, CINC-1 and MCP-1, as well as using eosin hematoxylin staining. Furthermore, MPO activity and MCP-1 and CINC-1 concentrations of tissue homogenates were measured. All differences were analyzed statistically using the Mann-Whitney U-test. Results: During HS infusion, a rapid influx of macrophages/monocytes, as visualized as ED-1 positive cells, was seen reaching a maximum at 6 hours. After 48 hours, the same levels of ED-1 positive cells were noted in the pancreatic tissue, but with different location and morphology. Increased neutrophil numbers of heparan sulphate treated animals compared to control could be detected only 9 hours after infusion. The number of neutrophils was lower than the number of ED-1 positive cells. On the contrary, LPS infusion caused increased neutrophil numbers to a larger extent than heparan sulphate. Furthermore, this accumulation of neutrophils preceded the infiltration of ED-1 positive cells. Chemokine expression correlates very well to the cell infiltrate. MCP-1 was evident in the ductal cells of both groups early on. MCP-1 preceded monocyte infiltration in both groups, while the CINC-1 increase was only noticeable in the LPS group. Conclusions: Our data suggest that heparan and LPS both induce host defense reactions, though by using different mechanisms of cell-recruitment. This implies that the etiology of pancreatic inflammation may influence how the subsequent events will develop.

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Akbarshahi, HamidLund University,Lunds universitet,Kirurgi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Surgery (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)med-hab (author)
Said Hilmersson, KatarzynaLund University,Lunds universitet,Kirurgi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Surgery (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)oft-ksa (author)
Malmström, AndersLund University,Lunds universitet,Matrixbiologi,Forskargrupper vid Lunds universitet,Matrix Biology,Lund University Research Groups(Swepub:lu)medk-ama (author)
Andersson, RolandLund University,Lunds universitet,Kirurgi, Lund,Sektion V,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Surgery (Lund),Section V,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)kir-ran (author)
MatrixbiologiForskargrupper vid Lunds universitet (creator_code:org_t)

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