Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the Rat

In this work we have studied the acute phase protein response and degranulation of polymorphonuclear leukocytes in vivo in the rat after a slow interleukin-1β stimulation. A total dose of 1 μg, 2 μg, 4 μg and 0 μg (controls with only vehicle) of interleukin-1β was released from osmotic minipumps ove...

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Main Authors: Peter Björk, Thorarinn Gudmundsson, Kjell Ohlsson
Format: Article
Language:English
Published: Wiley 1994-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/S0962935194000608
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author Peter Björk
Thorarinn Gudmundsson
Kjell Ohlsson
author_facet Peter Björk
Thorarinn Gudmundsson
Kjell Ohlsson
author_sort Peter Björk
collection DOAJ
description In this work we have studied the acute phase protein response and degranulation of polymorphonuclear leukocytes in vivo in the rat after a slow interleukin-1β stimulation. A total dose of 1 μg, 2 μg, 4 μg and 0 μg (controls with only vehicle) of interleukin-1β was released from osmotic minipumps over a period of 7 days. The pumps were implanted subcutaneously. A cystic formation was formed around the pumps that contained interleukin-1β whereas no tissue reaction was seen around pumps containing only vehicle. Besides flbroblasts the cyst wall contained numerous polymorphonuclear leukocytes which were positively stained for cathespin G. α2-macroglobulin, α1-inhtbitor-3, α1-proteinase inhibitor, albumin and C3 were measured by electroimmunoassay and all showed plasma concentration patterns that were dose-dependent to the amount of interleuktn-1β released. Fibrinogen in plasma was elevated in the control group but showed decreased plasma values with higher doses of interleukin-1β released. All animals showed increased plasma levels of cathespin G but the lowest levels for cathespin G were seen for the highest interleukin-1β dose released. It was clearly seen that a slow continuous release of interleukin-1β in vivo caused an inflammatory reaction. Plasma levels for the proteins analysed all showed a similar pattern, namely an initial increase or decrease of plasma concentration followed by a tendency to normalization of plasma values. It was concluded that a long-term interleukin-1β release could not sustain the acute phase protein response elicited by the initial interleukin-1β release.
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spelling doaj-art-24aa725a0f3244dfb7e6f007d2bef1162025-08-20T02:04:40ZengWileyMediators of Inflammation0962-93511466-18611994-01-013642543110.1155/S0962935194000608Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the RatPeter Björk0Thorarinn Gudmundsson1Kjell Ohlsson2Department of Surgical Pathophysiology, University of Lund, Malmö General Hospital, Malmö S-214 01, SwedenDepartment of Surgical Pathophysiology, University of Lund, Malmö General Hospital, Malmö S-214 01, SwedenDepartment of Surgical Pathophysiology, University of Lund, Malmö General Hospital, Malmö S-214 01, SwedenIn this work we have studied the acute phase protein response and degranulation of polymorphonuclear leukocytes in vivo in the rat after a slow interleukin-1β stimulation. A total dose of 1 μg, 2 μg, 4 μg and 0 μg (controls with only vehicle) of interleukin-1β was released from osmotic minipumps over a period of 7 days. The pumps were implanted subcutaneously. A cystic formation was formed around the pumps that contained interleukin-1β whereas no tissue reaction was seen around pumps containing only vehicle. Besides flbroblasts the cyst wall contained numerous polymorphonuclear leukocytes which were positively stained for cathespin G. α2-macroglobulin, α1-inhtbitor-3, α1-proteinase inhibitor, albumin and C3 were measured by electroimmunoassay and all showed plasma concentration patterns that were dose-dependent to the amount of interleuktn-1β released. Fibrinogen in plasma was elevated in the control group but showed decreased plasma values with higher doses of interleukin-1β released. All animals showed increased plasma levels of cathespin G but the lowest levels for cathespin G were seen for the highest interleukin-1β dose released. It was clearly seen that a slow continuous release of interleukin-1β in vivo caused an inflammatory reaction. Plasma levels for the proteins analysed all showed a similar pattern, namely an initial increase or decrease of plasma concentration followed by a tendency to normalization of plasma values. It was concluded that a long-term interleukin-1β release could not sustain the acute phase protein response elicited by the initial interleukin-1β release.http://dx.doi.org/10.1155/S0962935194000608
spellingShingle Peter Björk
Thorarinn Gudmundsson
Kjell Ohlsson
Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the Rat
Mediators of Inflammation
title Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the Rat
title_full Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the Rat
title_fullStr Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the Rat
title_full_unstemmed Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the Rat
title_short Acute Phase Protein Response and Polymorphonuclear Leukocyte Cathepsin G Release After Slow Interleukin-1 Stimulation in the Rat
title_sort acute phase protein response and polymorphonuclear leukocyte cathepsin g release after slow interleukin 1 stimulation in the rat
url http://dx.doi.org/10.1155/S0962935194000608
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