3763 Differential Induction of Cytokines by Candida albicans
K. PABST, W. JUMPER, M.J. PABST, and J.P. BABU, University of Tennessee, Memphis, USA

Virulence of Candida albicans in denture-induced stomatitis has been attributed to successful colonization and formation of a biofilm on denture acrylic material. Additionally, selective induction of monocyte cytokines by C. albicans might play role in pathogenesis in the oral cavity. Objective: To compare the monocyte cytokine-inducing ability of liquid-cultured C. albicans with C. albicans obtained from a biofilm. Methods: C. albicans ATCC 44505 and 28366 strains were used in this study. They were grown in liquid culture media and also isolated from an artificially created biofilm. Mononuclear cells were isolated from human blood, cultured at 37C in Teflon bags, and exposed to C. albicans (1,000 to 500,000 cells) for 18 h. The culture supernatants were collected, and assayed for IL-1b, TNFa, and IL-12, using ELISA kits (R&D Systems). Results: IL-1b and TNFa levels were higher in media from monocytes exposed to biofilm C. albicans, compared with C. albicans grown in liquid medium, whereas IL-12 levels were lower (P<0.001 by ANOVA). The magnitude of the cytokine response increased with increasing numbers of C. albicans added (P<0.001). There was also a difference between the two strains of C. albicans (P<0.001). For example, IL-1b induced by 500,000 biofilm C. albicans 44805 (1836 51 pg/ml, mean  SE, n = 3) was significantly greater than the same yeasts grown in liquid form (1579 63 pg/ml). Conclusion: Biofilm growth conditions alter the ability of C. albicans to induce cytokines from monocytes. The ability of C. albicans, particularly in biofilm form, to induceIL-1b and TNFa, and to suppress IL-12 production by monocytes, might promote inflammation and increase the susceptibility of the host to candidiasis.

Supported by DE05494 and DE07258

Seq #377 - Cytokines/Growth Factors/Matrix Enzymes
10:15 AM-11:30 AM, Saturday, 13 March 2004 Hawaii Convention Center Exhibit Hall 1-2

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