Anti-CD14 antibodies reduce responses of cultured human endothelial cells to endotoxin

Lipopolysaccharide (LPS) activates both myeloid and endothelial cells. Whereas CD14 has been shown to be involved in LPS recognition by myeloid cells, the mechanism responsible for the strong response of endothelial cells to LPS remains to be elucidated. The role of CD14 in this process was studied...

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Bibliographic Details
Published in:Immunology 1993-09, Vol.80 (1), p.78-83
Main Authors: VON ASMUTH, E. J. U, DENTENER, M. A, BAZIL, V, BOUMA, M. G, LEEUWENBERG, J. F. M, BUURMAN, W. A
Format: Article
Language:English
Subjects:
Animal cells
Antibodies - immunology
Antigens, CD - immunology
Antigens, Differentiation, Myelomonocytic - immunology
Biological and medical sciences
Cell Adhesion Molecules - immunology
Cell cultures. Hybridization. Fusion
Cells, Cultured
E-Selectin
Endothelium - cytology
Endothelium - immunology
Endotoxins - immunology
Fundamental and applied biological sciences. Psychology
Humans
Interleukin-6 - immunology
Lipopolysaccharide Receptors
Lipopolysaccharides - immunology
Molecular and cellular biology
Monocytes - immunology
Receptors, Immunologic - immunology
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Summary:Lipopolysaccharide (LPS) activates both myeloid and endothelial cells. Whereas CD14 has been shown to be involved in LPS recognition by myeloid cells, the mechanism responsible for the strong response of endothelial cells to LPS remains to be elucidated. The role of CD14 in this process was studied using CD14-specific antibodies (Ab). Anti-CD14 Ab inhibited LPS-induced interleukin-6 (IL-6) release and E-selectin expression by cultured human umbilical vein endothelial cells (HUVEC). Messenger RNA encoding IL-6 and E-selectin was reduced in parallel. The inhibitory effect of anti-CD14 Ab was epitope dependent, maximal at low LPS concentrations and dropping with increasing LPS doses. Anti-CD14 Ab did not affect endothelial cell activation induced by IL-1 beta, tumour necrosis factor-alpha (TNF-alpha) and phorbol 12-myristate 13-acetate (PMA). IL-6 release and E-selectin expression of HUVEC were strongly reduced when LPS activation was performed in the absence of serum, indicating involvement of serum components in LPS activation of HUVEC. Nevertheless, anti-CD14 Ab also blocked LPS-induced HUVEC activation in the absence of serum. Although the role of serum components in LPS activation remains to be elucidated, CD14 seems to be a key mediator in LPS-induced activation of endothelial cells.
ISSN:0019-2805
1365-2567