INTERACTIONS BETWEEN CANDIDA SPECIES AND PLATELETS

Candida spp. are able to cause disseminated disease in immunocompromis ed patients. This study examined the interactions of Candida spp. with platelets, complement and polymorphonuclear leucocytes (PMNLs). With the exception of C. albicans, all other Candida spp., including a C. a lbicans strain previously classified as C. stellatoidia, aggregated hu man platelets at a ratio of yeast cells: platelets of 1:80. Usually, t hose species and strains that aggregated platelets were either killed or prevented from growing in platelet-rich plasma indicating that the aggregation released microbicidal or microbistatic substances that wer e active against Candida spp. All Candida spp. were resistant to attac k by complement in 50% serum. However, all species activated complemen t as determined by the presence of C3 fragments on their surface, in p articular a 195-kDa fragment corresponding to C3c, two fragments at 67 and 40 kDa corresponding to iC3b, and a 33-kDa fragment corresponding to C3d. When strains were tested for their ability to stimulate the r elease of pro-inflammatory substances from platelets and PMNLs, it was found that most strains stimulated PMNLs to release interleukin(IL)-8 but not IL-1 beta or leucotriene B-4. The ability of C. albicans to e vade complement-mediated killing and not to aggregate platelets may co ntribute to the survival of this species in the blood during vascular infections.