Cytokine production during hemodialysis: effects of dialytic membrane and complement activation.
Interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) are closely associated with acute and chronic inflammatory processes in hemodialytic patients. However, the mechanisms concerning cytokine production by monocytes during hemodialysis are still conflicting. With the use of the more specific monoclonal antibody ELISA method, contamination detection and crossover protocol of complement-activating and noncomplement-activating hollow fibers, we were able to confirm augmented II-1 beta production by zymosan-stimulated monocytes with complement-activating hollow fiber as compared to noncomplement-activating hollow fiber before (1,411.9 +/- 865.7 +/- 149.9 pg/ ml/2 x 10(6) monocytes, p < 0.01). at the 15th minute (530.6 +/- 89.1 vs. 247.3 +/- 45.2 pg/ml/2 x 10(6) monocytes, p < 0.01) and at the end of dialysis (1,201.8 +/- 135.1 vs. 707.4 +/- 109.3 pg/ml/2 x 10(6) monocytes, p < 0.01). Similar results were observed with TNF-alpha production. IL-1 beta as well as TNF-alpha production decreased significantly at the 15th min of dialysis, thereafter they increased and approached the baseline levels towards the end of hemodialysis with both hollow fibers. Plasma C3a at the 15th minute correlated positively with postdialysis IL-1 beta and TNF-alpha production, while plasma C3a did not change in patients dialyzed with noncomplement-activating hollow fiber. Complement activation with complement-activating hollow fiber as well as monocyte-membrane interaction with complement-activating and noncomplement-activating hollow fiber might be involved in the pathogenesis of cytokine production during hemodialysis. Uremic toxin removal as well as stimulation of cytokine production inhibitor might contribute to the decreased cytokine production at the 15th minute of hemodialysis and monocyte-membrane interaction with or without complement activation resulted in augmented cytokine production toward the end of hemodialysis with both hollow fibers. We thus concluded that hollow fiber of bioincompatibility triggered much more cytokine production throughout the dialysis procedure.
Lin
Y F
YF
Division of Nephrology, Tri-Service General Hospital, Taipei, Taiwan.
Chang
D M
DM
Shaio
M F
MF
Lu
K C
KC
Chyr
S H
SH
Li
B L
BL
Sheih
S D
SD
D002482:Cellulose / Q000031:analogs & derivatives; D003167:Complement Activation; D015926:Complement C3a / Q000032:analysis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis*; D008297:Male; D008567:Membranes, Artificial; D008768:Methylmethacrylates; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D006435:Renal Dialysis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*; D014511:Uremia / Q000276:immunology / Q000378:metabolism / Q000628:therapy
D007375:Interleukin-1; D008567:Membranes, Artificial; D008768:Methylmethacrylates; D014409:Tumor Necrosis Factor-alpha; D015926:Complement C3a; D002482:Cellulose; C009865:cuprammonium cellulose