Chronic mucocutaneous candidiasis (CMC) is a group of
disorders, characterised by persistent mucocutaneous
infections with Candida species. The underlying defect of CMC has not been elucidated, but a defective cytokine response may be involved. Therefore, we investigated whether an imbalance between IFNã and IL-10 may play a role in this disorder.
We assessed the cytokine production in whole-blood
cultures from CMC patients using Candida albicans, lipopolysaccharide and phytohaemagglutinin as stimuli.
As the Toll-like receptors are important pattern recognition receptors for Candida species, we also investigated Toll-like receptor polymorphisms in these patients.
Patients with CMC had a significantly decreased IFNã production when whole blood was stimulated with C.
albicans (232 ± 120 vs 2279 ± 609 pg/ml, p<0.02). When stimulated with phytohaemagglutinin, the differences were not significant (3549 ± 1320 vs 7631 ± 1790 pg/ml).
The Candida-stimulated production of IL-10 tended to be higher in CMC patients, whereas TNF and IL-1beta; production were similar in patients and controls. Stimulation with LPS showed no differences in cytokine production between patients and controls. Two out of seven patients had the TLR4 Asp299Gly polymorphism and none had the TLR2 Arg677Trp polymorphism.
These data support the hypothesis that deficient IFNã production is involved in the pathogenesis of CMC,
whereas a role for genetic polymorphisms of Toll-like
receptor 2 and 4 is not obvious in these patients.