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Infection and Immunity, March 2001, p. 1273-1279, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1273-1279.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Bacterial Lipopolysaccharide and Tumor Necrosis Factor Alpha Synergistically Increase Expression of Human Endothelial Adhesion Molecules through Activation of NF-kappa B and p38 Mitogen-Activated Protein Kinase Signaling Pathways

Hubertus P. A. Jersmann,dagger Charles S. T. Hii, Judith V. Ferrante, and Antonio Ferrante*

Department of Immunopathology, The Women's and Children's Hospital, North Adelaide, South Australia 5006, and Department of Paediatrics, University of Adelaide, Adelaide, South Australia 5000, Australia

Received 19 June 2000/Returned for modification 18 September 2000/Accepted 22 November 2000

One of the recognized associations of bacterial infection with cardiovascular events is the activation of endothelium and upregulation of adhesion molecules. The two major proinflammatory mediators implicated in the causation of cardiovascular events, bacterial lipopolysaccharide (LPS) and tumor necrosis factor alpha (TNF), were found to cooperate to enhance the adhesive properties of endothelial cells. These caused synergistic upregulation of intercellular adhesion molecule-1, E-selectin, and vascular cell adhesion molecule-1 in human umbilical vein endothelial cells as determined by flow cytometry analysis and enzyme-linked immunosorbent assay. This synergism was not due to TNF causing an upregulation of CD14 expression. Treatment with both LPS and TNF resulted in a marked increase in the translocation of NF-kappa B into the nucleus. The activity of p38 mitogen-activated protein kinase was also synergistically enhanced, while the activity of c-jun N-terminal kinase was increased in an additive manner. The results demonstrate that LPS and TNF act synergistically to upregulate the expression of endothelial cell adhesion molecules, possibly by amplification of signaling pathways upstream of transcription. These findings have implications for the understanding of the acceleration of atherosclerotic events seen in low-grade infections with gram-negative organisms.

* Corresponding author. Mailing address: Department of Immunopathology, The Women's and Children's Hospital, 72 King William Rd., North Adelaide, South Australia 5006, Australia. Phone: 61 8 8204 7216. Fax: 61 8 8204 6046. E-mail: aferrant{at}medicine.adelaide.edu.au.

dagger Present addresses: Respiratory Medicine Unit, Rayne Laboratory, University of Edinburgh Teviot Place, Edinburgh EH8 9AG, United Kingdom.

Infection and Immunity, March 2001, p. 1273-1279, Vol. 69, No. 3
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.3.1273-1279.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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