Advanced oxidation protein products as novel mediators of inflammation and monocyte activation in chronic renal failure

We previously demonstrated the presence of advanced oxidation protein products (AOPP), a novel marker of oxidative stress in the plasma of uremic patients receiving maintenance dialysis. The present study in a cohort of 162 uremic patients showed that plasma concentrations of AOPP increased with pro...

Full description

Saved in:
Bibliographic Details
Published in:The Journal of immunology (1950) 1998-09, Vol.161 (5), p.2524-2532
Main Authors: Witko-Sarsat, V, Friedlander, M, Nguyen Khoa, T, Capeillère-Blandin, C, Nguyen, A T, Canteloup, S, Dayer, J M, Jungers, P, Drüeke, T, Descamps-Latscha, B
Format: Article
Language:English
Subjects:
Adult
Biomarkers - blood
Cytokines - blood
Glycation End Products, Advanced - blood
Humans
Inflammation - blood
Inflammation - immunology
Kidney Failure, Chronic - blood
Kidney Failure, Chronic - immunology
Kidney Failure, Chronic - pathology
Macrophage Activation - drug effects
Monocytes - immunology
Monocytes - metabolism
Oxidative Stress - immunology
Respiratory Burst - drug effects
Respiratory Burst - immunology
Serum Albumin - physiology
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:We previously demonstrated the presence of advanced oxidation protein products (AOPP), a novel marker of oxidative stress in the plasma of uremic patients receiving maintenance dialysis. The present study in a cohort of 162 uremic patients showed that plasma concentrations of AOPP increased with progression of chronic renal failure and were closely related to advanced glycation end products (AGE)-pentosidine (r = 0.52, p < 0.001), taken as a marker of AGE. In vivo, the relevance of AOPP and AGE-pentosidine in monocyte-mediated inflammatory syndrome associated with uremia was evidenced by close correlations between AOPP or AGE-pentosidine and monocyte activation markers, including neopterin, IL-1R antagonist, TNF-alpha, and TNF soluble receptors (TNF-sR55 and TNF-sR75). To determine the mechanisms by which AOPP and AGE could be directly involved in monocyte activation, AOPP-human serum albumin (HSA) and AGE-HSA were produced in vitro by treating HSA with oxidants or glucose, respectively. Spectroscopic analysis confirmed that AOPP-HSA contains carbonyls and dityrosine. Both AOPP-HSA and AGE-HSA, but not purified dityrosine, were capable of triggering the oxidative burst of human monocytes in cultures. The AOPP-HSA-induced respiratory burst was dependent on the chlorinated nature of the oxidant and on the molar ratio HSA/HOCI. Collectively, these data first demonstrate that AOPP act as a mediator of oxidative stress and monocyte respiratory burst, which points to monocytes as both target and actor in the immune dysregulation associated with chronic uremia.
ISSN:0022-1767