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Interleukin‐1α, interleukin 6 and tumor necrosis factor α increase the synthesis and expression of the functional alternative and terminal complement pathways by human umbilical vein endothelial cells in vitro
Author(s) -
BERGE V.,
JOHNSON E.,
BERGE K. E.
Publication year - 1996
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1996.tb00710.x
Subject(s) - proinflammatory cytokine , tumor necrosis factor alpha , complement system , interleukin , cytokine , umbilical vein , antibody , alternative complement pathway , immunology , biology , chemistry , microbiology and biotechnology , in vitro , inflammation , biochemistry
The proinflammatory cytokines interleukin la (IL‐1α), tumor necrosis factor a (TNFa) and interleukin 6 (IL‐6) modulate the synthesis of complement factors B and C3 by endothelial cells (EC), and are considered to play an important role in the development of sepsis. By using agarose beads activating the alternative pathway of complement, we wanted to study the net effect of these cytokines on EC synthesis of the alternative and terminal pathways, measured by binding of anti‐C3c and anti‐TCC (terminal complement complex) antibodies to beads kept with the EC. Addition of IL‐1α and TNFa at concentrations of 50 and 100 U/ml resulted in a significant increase in binding of these antibodies to co‐incubated beads, most pronounced for anti‐C3c. IL‐6 from 50–200 U/ml resulted in a stronger (two to fourfold) binding for both antibodies compared to experiments with IL‐la and TNF. However, increased concentrations of IL‐la (200 U/ml) and IL‐6 (400 U/ml) resulted in a strong reduction in binding of anti‐C3c and anti‐TCC antibodies to the co‐cultured beads. This study indicates that proinflammatory cytokines upregulate the synthesis by EC of the functional alternative and terminal pathways of complement.