Changes in the serum concentration and the glycosylation of human αl‐acid glycoprotein and αl‐protease inhibitor in severely burned persons: relation to interleukin‐6 levels

SUMMARY The relation between interleukin‐6 (TL‐6) levels and changes in serum concentrations and glycosylation (concanavalin A affinity) of two human acute‐phase glycoproteins, αl‐acid glycoprotein (AGP) and α1‐protease inhibitor (PI), was studied in sequential serum samples of burn patients. The le...

Full description

Saved in:
Bibliographic Details
Published in:Clinical and experimental immunology Vol. 82; no. 3; pp. 579 - 582
Main Authors: POS, O., STELT, M. E., WOLBINK, G.‐J., NUSTEN, M. W. N., TEMPEL, G. L., DIJK, W.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 28-06-2008
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:SUMMARY The relation between interleukin‐6 (TL‐6) levels and changes in serum concentrations and glycosylation (concanavalin A affinity) of two human acute‐phase glycoproteins, αl‐acid glycoprotein (AGP) and α1‐protease inhibitor (PI), was studied in sequential serum samples of burn patients. The level of IL‐6 was already increased at the first day following injury, and after a dip at day 2 or 3 rapidly reached a second maximal value at day 4 or 5. The serum concentrations of AGP and PI reached their maximal values after day 5 and remained at a high level throughout the total period studied (7 weeks). The concanavalin A reactivities of both acute‐phase glycoproteins were found to be elevated only during the first 2–25 weeks. Maximal values were observed on day 2 and from day 7 to 16, following closely the rise and fall of the lL‐6 serum level. After day 16, the concanavalin A affinity rapidly declined long before a decrease was observed in the serum concentrations of AGP and PI. Our previous in vitro studies have indicated an involvement of lL‐6 in the induction of both secretion and increased concanavalin A affinity. This study indicates that IL‐6 could play a causal role in the induction of both phenomena in vivo.
Bibliography:O.P. present address: Department of Infectious Diseases, University Hospital, Leiden, The Netherlands.
ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.1990.tb05493.x