Interactions between Candida species and platelets.
Candida spp. are able to cause disseminated disease in immunocompromised 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. albicans strain previously classified as C. stellatoidia, 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 Candida spp. All Candida 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-1beta or leucotriene B4. The ability of C. albicans to evade complement-mediated killing and not to aggregate platelets may contribute to the survival of this species in the blood during vascular infections.
Willcox
M D
MD
Cornea and Contact Lens Research Unit, School of Optometry and Cooperative Research Centre for Eye Research and Technology, University of New South Wales, Australia.
Webb
B C
BC
Thakur
A
A
Harty
D W
DW
D000925:Anticoagulants / Q000494:pharmacology; D001081:Apyrase / Q000494:pharmacology; D001792:Blood Platelets / Q000382:microbiology*; D002175:Candida / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D002478:Cells, Cultured; D003167:Complement Activation; D003165:Complement System Proteins / Q000276:immunology*; D004492:Edetic Acid / Q000494:pharmacology; D006801:Humans; D007099:Imipramine / Q000494:pharmacology; D007375:Interleukin-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D009504:Neutrophils / Q000382:microbiology*; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D011796:Quinacrine / Q000494:pharmacology
D000925:Anticoagulants; D007375:Interleukin-1; D016209:Interleukin-8; D010975:Platelet Aggregation Inhibitors; D003165:Complement System Proteins; D004492:Edetic Acid; D001081:Apyrase; D011796:Quinacrine; D007099:Imipramine