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Infection and Immunity, December 2002, p. 7073-7080, Vol. 70, No. 12
0019-9567/02/$04.00+0 DOI: 10.1128/IAI.70.12.7073-7080.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Faculté de médecine dentaire,1 GREB,2 Centre de recherche, Institut universitaire de cardiologie et de pneumologie, Hôpital Laval, Université Laval, Québec G1K 7P4, Canada3
Received 5 June 2002/ Returned for modification 29 July 2002/ Accepted 27 August 2002
Oral candidiasis is a collective name for a group of disorders caused by the dimorphic fungus Candida albicans. Host defenses against C. albicans essentially fall into two categories: specific immune mechanisms and local oral mucosal epithelial cell defenses. Since oral epithelial cells secrete a variety of cytokines and chemokines in response to oral microorganisms and since C. albicans is closely associated with oral epithelial cells as a commensal organism, we wanted to determine whether interleukin-18 (IL-18) and gamma interferon (IFN-
) were produced by oral epithelial cells in response to C. albicans infection and lipopolysaccharide (LPS) stimulation. Our results showed that IL-18 mRNA and protein were constitutively expressed by oral epithelial cells and were down-regulated by Candida infections but increased following LPS stimulation. Both C. albicans and LPS significantly decreased pro-IL-18 (24 kDa) levels and increased active IL-18 (18 kDa) levels. This effect was IL-1ß-converting-enzyme dependent. The increase in active IL-18 protein levels promoted the production of IFN-
by infected cells. No effect was obtained with LPS. Although produced only at an early stage, secreted IFN-
seemed to be a preferential response by oral epithelial cells to C. albicans growth. These results provide additional evidence for the contribution of oral epithelial cells to local (direct contact) and systemic (IL-18 and IFN-
production) defense against exogenous stimulation such as C. albicans infection or LPS stimulation.
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