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Infection and Immunity, March 2000, p. 1134-1141, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Mechanisms of the Proinflammatory Response of Endothelial Cells to Candida albicans Infection

Alison S. Orozco,1 Xiang Zhou,1 and Scott G. Filler1,2,*

St. John's Cardiovascular Research Center, Division of Infectious Diseases, Department of Internal Medicine, Harbor-UCLA Research and Education Institute, Torrance, California 90502,1 and UCLA School of Medicine, Los Angeles, California 900242

Received 16 August 1999/Returned for modification 15 November 1999/Accepted 1 December 1999

Endothelial cells can influence significantly the host inflammatory response against blood-borne microbial pathogens. Previously, we found that endothelial cells respond to in vitro infection with Candida albicans by secreting interleukin 8 (IL-8) and expressing E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1). We have now examined the mechanisms mediating this endothelial cell response. We determined that C. albicans stimulated endothelial cells to synthesize tumor necrosis factor alpha (TNF-alpha ), which in turn induced these infected cells to secrete IL-8 and express E-selectin by an autocrine mechanism. Expression of VCAM-1 was mediated not only by TNF-alpha but also by IL-1alpha and IL-1beta , all of which were synthesized by endothelial cells in response to C. albicans. These three cytokines remained primarily cell associated rather than being secreted. Candidal induction of ICAM-1 expression was independent of TNF-alpha , IL-1alpha , and IL-1beta . These observations demonstrate that different proinflammatory endothelial cell responses to C. albicans are induced by distinct mechanisms. A clear understanding of these mechanisms is important for therapeutically modulating the endothelial cell response to C. albicans and perhaps other opportunistic pathogens that disseminate hematogenously.

* Corresponding author. Mailing address: Division of Infectious Diseases, Harbor-UCLA Medical Center, 1000 West Carson St., RB-2, Torrance, CA 90509. Phone: (310) 222-6426. Fax: (310) 782-2016. E-mail: sfiller{at}ucla.edu.

Infection and Immunity, March 2000, p. 1134-1141, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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