Inflammation Induced by Candida parapsilosis in THP-1 Cells and Human Peripheral Blood Mononuclear Cells (PBMCs)

Candida parapsilosis is one of the most prevalent Candida species; however, the inflammation response induced by C. parapsilosis and related mechanism received few studies. In this study, we analyzed the pro-inflammatory cytokine responses evoked by C. parapsilosis in human peripheral blood mononuclear cells (PBMCs) and THP-1 cells, determined the signal pathways related to the inflammation response and investigated the expression of dectin-1 modified with C. parapsilosis. Exposure of PBMCs and THP-1 cells to C. parapsilosis led to the increased gene expression and production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). C. parapsilosis induced TNF-alpha and IL-6 release in a time- and dose-dependent manner. Western blotting was used to analyze p38, ERK1/2 mitogen-activated protein kinases (MAPKs) and I kappa B-alpha phosphorylation and degradation. Nuclear translocation of NF-kappa B was detected by confocal microscopy. THP-1 cells challenged by C. parapsilosis resulted in the activation of NF-kappa B and phosphorylation of p38 and ERK1/2 MAPKs. The expression of dectin-1 was up-regulated after the stimulation of C. parapsilosis. Our results suggest that C. parapsilosis could stimulate the inflammatory response, increase the expression of dectin-1 and activate NF-kappa B and MAPKs signaling pathways in macrophages.