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Nephrology Dialysis Transplantation, Vol 12, Issue 11 2365-2374, Copyright © 1997 by Oxford University Press

ORIGINAL ARTICLES

Dissociation between {beta}-2 microglobulin and IL-1 production in hemodialyzed patients

M Carreno, Y Rousseau, J Poignet, G Jahns, B Cholley, M Kazatchkine and N Haeffner-Cavaillon
INSERM U430, and Universite Pierre et Marie Curie, Hopital Broussais, 96 rue Didot, F-70514 Paris, France; Centre E Rist, Paris, France; Corresponding author

Background: {beta}-2 microglobulin is predominant in amyloid deposits in patients undergoing long term hemodialysis. Amyloid accumulation has been ascribed to dialysis membranes, endotoxin contamination of the dialysate, uremia and chronic systemic inflammation associated with enhanced monocytic cytokine production in hemodialyzed patients. Interleukin-1 has been proposed to play a critical role in the induction of {beta}-2 microglobulin synthesis and release. Methods: We examined if monocytes contribute to {beta}-2 microglobulin production upon stimulation with inflammatory mediators that are generated during hemodialysis and investigated the production of {beta}-2 microglobulin by cells from patients, with and without clinical signs of amyloidosis, at the time when patients' monocytes contained maximal intracellular accumulation of IL-2. Results: We demonstrated that only monocytes are able to release increased levels of {beta}-2 microglobulin upon stimulation by Il-1, TNF&agr;, C5a and LPS. Increased levels of {beta}-2 microglobulin were associated with increased levels of {beta}-2 microglobulin mRNA. Before dialysis session, 20-60% of circulating CD14+ monocytes from patients contained IL-2. At the time when maximal IL-1 production was detected, we showed by RT-PCR increased transcription of Il-1 gene in patients' monocytes. We observed that monocytes from patients with amyloidosis contained higher amounts of IL-1 as compared to monocytes from patients without clinical signs of amyloidosis, but could not secrete increased amounts of {beta}-2 microglobulin upon LPS-stimulation. Conclusions: Our data indicated that chronic inflammation, as demonstrated by increased intracellular IL-1 expression, is not associated with increased production of {beta}-2 microglobulin by monocytes from patients on hemodialysis. Key words: biocompatibility; hemodialysis, leukocytes, amyloidosis, cytokines
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