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Peripheral blood mononuclear cells induce programmed cell death in human
endothelial cells and may prevent repair: role of cytokines
H Lindner, E Holler, B Ertl, G Multhoff, M Schreglmann, I Klauke, S Schultz- Hector and G Eissner
Forschungszentrum fur Umwelt und Gesundheit-Institutes for Clinical
Molecular Biology, Hospital Grosshadern, Munich, Germany.
Human umbilical vein endothelial cells (HUVECs) undergo programmed cell
death (apoptosis) after coculture with peripheral blood mononuclear cells
(PBMCs) preactivated by ionizing radiation (IR) or by bacterial endotoxin
(lipopolysaccharide [LPS]). Cell-to-cell contact-mediated apoptosis could
be blocked in both cases by anti-tumor necrosis factor- alpha
(anti-TNF-alpha) monoclonal antibody MAK195 and also by the antagonistic
cytokine interleukin-10 (IL-10). Cell-free PBMC supernatants from both
preactivation treatments were sufficient to trigger endothelial apoptosis.
In contrast, MAK195 and IL-10 were found to be ineffective in this system,
suggesting a TNF-alpha-independent mechanism. However, N-Acetylcystein, an
antioxidant, fully abrogated programmed cell death mediated by the
supernatant of IR-treated PBMCs, but not of LPS-treated PBMCs.
Additionally, we found that coculture and cell-free supernatants of
preactivated as well as untreated PBMCs caused cell cycle arrest in
proliferating EC in G(0/1), which could be relieved by IL-10, but not by
anti-TNF-alpha. Further analysis showed that transforming growth
factor-beta, which was constitutively expressed in the supernatant of
PBMCs, namely lymphocytes, was responsible for this. These data suggest a
pathophysiologic model in which preactivated PBMCs cause EC damage and may
prevent blood vessel repair by arresting the proliferation of ECs. This
could contribute to the understanding of various clinical endothelial
complications that occur after irradiation as well as in cases of
endotoxemia or related inflammatory states.
Volume 89,
Issue 6,
pp. 1931-1938,
03/15/1997
Copyright © 1997 by The American Society of Hematology
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