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Infection and Immunity, February 2001, p. 897-905, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.897-905.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Human Endothelial Cell Activation and Mediator Release in Response to Listeria monocytogenes Virulence Factors

Frank Rose,1 Sven-Arne Zeller,1 Trinad Chakraborty,2 Eugen Domann,2 Thomas Machleidt,3 Martin Kronke,3 Werner Seeger,1 Friedrich Grimminger,1 and Ulf Sibelius1,*

Department of Internal Medicine1 and Institute of Medical Microbiology,2 Justus Liebig University, Giessen, and Institute of Microbiology, University of Cologne, Cologne,3 Germany

Received 17 April 2000/Returned for modification 8 July 2000/Accepted 15 November 2000

The interaction of Listeria monocytogenes with endothelial cells represents a crucial step in the pathogenesis of listeriosis. Incubation of human umbilical vein endothelial cells (HUVEC) with wild-type L. monocytogenes (EGD) provoked immediate strong NO synthesis, attributable to listerial presentation of listeriolysin O (LLO), as the NO release was missed upon employment of a deletion mutant for LLO (EGD hly mutant) and was reproduced by purified LLO. Studies of conditions lacking extracellular Ca2+ suggested LLO-elicited Ca2+ flux as the underlying mechanism. In addition, HUVEC incubation with EGD turned out to be a potent stimulus for sustained (>12-h) upregulation of proinflammatory cytokine generation (interleukin 6 [IL-6], IL-8, and granulocyte-macrophage colony-stimulating factor). Use of deletion mutants for LLO (EGD hly mutant), listerial phosphatidylinositol-specific phospholipase C (EGD plcA mutant), broad-spectrum phospholipase C (EGD plcB mutant) and internalin B (EGD inlB mutant), as well as purified LLO, identified LLO as largely responsible for the cytokine response. Endothelial cells responded with diacylglycerole and ceramide generation as well as nuclear translocation of NF-kappa B to the stimulation with the LLO-producing strains EGD and Listeria innocua. The endothelial PC-phospholipase C inhibitor tricyclodecan-9-yl-xanthogenate as well as two independent inhibitors of NF-kappa B activation, pyrolidine dithiocarbamate and caffeic acid phenethyl ester, suppressed both the NF-kappa B translocation and the upregulation of cytokine synthesis. We conclude that L. monocytogenes is a potent stimulus of NO release and sustained upregulation of proinflammatory cytokine synthesis in human endothelial cells, both events being largely attributable to LLO presentation. LLO-induced transmembrane Ca2+ flux as well as a sequence of endothelial phospholipase activation and the appearance of diacylglycerole, ceramide, and NF-kappa B are suggested as underlying host signaling events. These endothelial responses to L. monocytogenes may well contribute to the pathogenic sequelae in severe listerial infection and sepsis.

* Corresponding author. Mailing address: Department of Internal Medicine, Klinikstraße 36, D-35392 Giessen, Germany. Phone: 49-641-99-42351. Fax: 49-641-99-42359 or 49-641-99-42509. E-mail: ulf.sibelius{at}inn.med.uni-giessen.de.

Infection and Immunity, February 2001, p. 897-905, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.897-905.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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