Candida albicans induces the release of inflammatory mediators from human peripheral blood monocytes |
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Authors: | Mario Castro Julie A Bjoraker Michael S Rohrbach Andrew H Limper |
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Institution: | (1) Division of Pulmonary and Critical Care and Internal Medicine, Thoracic Diseases Research Unit, USA;(2) Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN |
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Abstract: | 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 -mannans and -glucans antagonize mannose and -glucan receptors, respectively. Preincubation of monocytes with -mannan (100 g/ml) caused 45.8 ±5.7% inhibition of 14C]-AA release, whereas -glucan (100 g/ml) yielded 43.7 ±6.0% inhibition (P<0.05 for each compared to control). Additionally, monocytes stimulated with C. albicans also released interleukin-1 (IL-1 ), tumor necrosis factor- (TNF ), interleukin-6 (IL-6) and interleukin-8 (IL-8). However, a-mannan or -glucan failed to inhibit IL-1 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 a-mannan and -glucan components of the fungus. |
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