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*
Department of Microbiology and Immunology, Division of Infectious Diseases,
Department of Medicine, and
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461
Cryptococcus neoformans is an encapsulated fungal
pathogen commonly acquired by inhalation. Extrapulmonary dissemination
can lead to infection of the bloodstream and various organs, most
commonly resulting in meningoencephalitis. However, infection with
C. neoformans is often characterized by a scant
inflammatory response. The leukocyte response to infection depends in
part upon a gradient of chemotactic factors and adhesion molecules
expressed by the host vascular endothelium, yet the inflammatory
response of human endothelial cells (EC) to C.
neoformans has not been previously investigated. We found that
incubation of primary human EC with C. neoformans did
not induce chemokine synthesis, and resulted in differential inhibition
of cytokine-induced IL-8, IFN-
-inducible protein-10, and monocyte
chemoattractant protein-1. In contrast, C. neoformans
had little effect on EC surface expression of the leukocyte ligand,
ICAM-1, as determined by flow cytometry. Modulation of chemokine
production was dependent on the chemokine under study, the inoculum of
C. neoformans used, fungal viability, and cell-cell
contact, but independent of cryptococcal strain or encapsulation. These
observations suggest a novel mechanism whereby C.
neoformans can affect EC function and interfere with the host
inflammatory response.
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