1887

Abstract

spp. are able to cause disseminated disease in immunocompromised patients. This study examined the interactions of spp. with platelets, complement and polymorphonuclear leucocytes (PMNLs). With the exception of , all other spp., including a strain previously classified as , aggregated human platelets at a ratio of yeast cells: platelets of 1:80. Usually, those 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 were active against spp. All spp. were resistant to attack by complement in 50% serum. However, all species activated complement as determined by the presence of C3 fragments on their surface, in particular 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 release 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 or leucotriene B. The ability of to evade complement-mediated killing and not to aggregate platelets may contribute to the survival of this species in the blood during vascular infections.

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1998-02-01
2024-04-19
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