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Published on: December 10, 2013
Inflammation Induced by Candida parapsilosis in THP-1 Cells and Human Peripheral Blood Mononuclear Cells (PBMCs)
Zhimin Duan1, Xu Chen1, Leilei Du1
1Institute of Dermatology, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Chinese Academy of Medical Science & Peking Union Medical College, 12 Jiang Wang Miao Street, Nanjing, 210042, People's Republic of China.
Abstract:
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-α (TNF-α) and interleukin-6 (IL-6). C. parapsilosis induced TNF-α 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 IκB-α phosphorylation and degradation. Nuclear translocation of NF-κB was detected by confocal microscopy. THP-1 cells challenged by C. parapsilosis resulted in the activation of NF-κB 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-κB and MAPKs signaling pathways in macrophages.
Insights
Candida parapsilosis triggers inflammation by increasing pro-inflammatory cytokines like TNF-α and IL-6. This fungus also upregulates dectin-1 and activates key signaling pathways, including NF-κB and MAPKs, in immune cells.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Candida parapsilosis is a common fungal species, but mechanisms of its induced inflammation are understudied.
- Understanding C. parapsilosis-mediated immune responses is crucial for managing associated infections.
Purpose of the Study:
- To analyze pro-inflammatory cytokine responses to C. parapsilosis in human immune cells.
- To determine the signaling pathways involved in C. parapsilosis-induced inflammation.
- To investigate the role of dectin-1 in the host response to C. parapsilosis.
Main Methods:
- Human peripheral blood mononuclear cells (PBMCs) and THP-1 cells were exposed to C. parapsilosis.
- Gene expression and cytokine production (TNF-α, IL-6) were measured.
- Western blotting assessed MAPK and NF-κB pathway activation.
- Confocal microscopy detected NF-κB nuclear translocation.
- Dectin-1 expression was analyzed post-stimulation.
Main Results:
- C. parapsilosis exposure increased TNF-α and IL-6 gene expression and production in a time- and dose-dependent manner.
- Activation of NF-κB and phosphorylation of p38 and ERK1/2 MAPKs were observed in THP-1 cells.
- Dectin-1 expression was upregulated following C. parapsilosis stimulation.
- C. parapsilosis induced inflammatory cytokine release and pathway activation in macrophages.
Conclusions:
- C. parapsilosis effectively stimulates pro-inflammatory cytokine production.
- The fungus activates NF-κB and MAPK signaling pathways.
- Dectin-1 expression is enhanced by C. parapsilosis, suggesting its involvement in the immune recognition.
- These findings elucidate key mechanisms of C. parapsilosis-induced inflammation.
