Importance of the terminal complement components for immune defence against Candida.
Candida activates complement via all three pathways leading to opsonisation and anaphylaxis. The aim of the study was to investigate the influence of the terminal complement system on Candida infections. Thus, fungal cell growth, mitochondrial activity and phagocytosis by polymorphonuclear leukocytes (PMNLs) as well as specific virulence factors, such as release of secreted aspartic protease (Sap) and adherence to epithelial cells, were assessed under the influence of normal or C6/C7-depleted serum. Candida (C.) dubliniensis was used in all experiments as prototype because of its known increased expression of Saps and its strong geno- and phenotypical similarity to the most abundant Candida species C. albicans. Being exposed to sufficient quantities of complement, fungal growth decreased and phagocytosis increased but mitochondrial activities of the yeast increased as well. Concerning the virulence factors, both adhesion and especially Sap release were markedly reduced in the presence of high serum concentrations. Interestingly, at low serum concentrations some opposite effects (an augmented cell growth, a higher Sap release and a stronger adhesion) were observed. In particular, it was shown that the presence of terminal complement factors, and thus the generation of the membrane attack complex, clearly induced a higher fungal mitochondrial activation and has an effect on host defence against yeast cells by augmenting phagocytosis.
Triebel
Till
T
Institut für Hygiene & Sozialmedizin, University of Innsbruck, Innsbruck, Austria.
Grillhösl
Barbara
B
Kacani
Laco
L
Lell
Claudia P
CP
Fuchs
Anita
A
Speth
Cornelia
C
Lass-Flörl
Cornelia
C
Steinmann
Jörg
J
Dierich
Manfred P
MP
Würzner
Reinhard
R
D002175:Candida / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity*; D002177:Candidiasis / Q000276:immunology* / Q000382:microbiology; D002448:Cell Adhesion; D003167:Complement Activation; D003183:Complement C6 / Q000172:deficiency / Q000276:immunology*; D003184:Complement C7 / Q000172:deficiency / Q000276:immunology*; D006367:HeLa Cells; D006801:Humans; D007113:Immunity, Innate; D009504:Neutrophils / Q000276:immunology; D010587:Phagocytosis; D014774:Virulence
D003183:Complement C6; D003184:Complement C7