Candida albicans (C. albicans) is a major nosocomial pathogen. We examined arachidonic acid (AA) and cytokine production by monocytes stimulated with C. albicans. [ 14C]-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 that soluble α-mannans and β-glucans antagonize mannose and β-glucan receptors, respectively. Preincubation of monocytes with α-mannan (100 μg/ml) caused 45.8 ± 5.7% inhibition of [ 14C]-AA release, whereas β-glucan (100 μg/ml) yielded 43.7 ± 6.0% inhibition (P < 0.05 for each compared to control). Additionally, monocytes stimulated with C. albicans also released interleukin-1β (IL-1β), tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and interleukin-8 (IL-8). However, α-mannan or β-glucan failed to inhibit IL-1β release. These data indicate that C. albicans induces monocytes to release AA and inflammatory cytokines. Furthermore, AA, but not cytokine liberation, is partially mediated by α-mannan and β-glucan components of the fungus.