CANDIDA-ALBICANS INDUCES THE RELEASE OF INFLAMMATORY MEDIATORS FROM HUMAN PERIPHERAL-BLOOD MONOCYTES

Candida albicans (C. albicans) is a major nosocomial pathogen. We exam ined arachidonic acid (AA) and cytokine production by monocytes stimul ated with C. albicans. [C-14]-AA labeled monocytes released 8.9 +/- 2. 3% of the incorporated AA following stimulation with live C. albicans (C. albicans: monocyte of 16:1) (P = 0.0002). Prior studies indicate t hat soluble alpha-mannans and beta-glucans antagonize mannose and beta -glucan receptors, respectively. Preincubation of monocytes with alpha -mannan (100 mu g/ml) caused 45.8 +/- 5.7% inhibition of [C-14]-AA rel ease, whereas beta-glucan (100 mu g/ml) yielded 43.7 +/- 6.0% inhibiti on (P < 0.05 for each compared to control). Additionally, monocytes st imulated with C. albicans also released interleukin-1 beta (IL-1 beta) , tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and in terleukin-8 (IL-8). However, alpha-mannan or beta-glucan failed to inh ibit IL-1 beta release. These data indicate that C. albicans induces m onocytes to release AA and inflammatory cytokines. Furthermore, AA, bu t not cytokine liberation, is partially mediated by alpha-mannan and b eta-glucan components of the fungus.