ArticleMycopathologia2017
Inflammation Induced by Candida parapsilosis in THP-1 Cells and Human Peripheral Blood Mononuclear Cells (PBMCs).
Article in Mycopathologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Clec7a Drives Microglial Activation-Mediated Myelin Degradation in Sepsis-Associated Encephalopathy.Inflammation · 2026Article
- The Fecal Mycobiome in Chronic Pancreatitis Is Characterized by an Increase in Candida species and Nakaseomyces.Clinical and translational gastroenterology · 2025Article
- Nanoceria Anti-inflammatory and Antimicrobial Nanodrug: Cellular and Molecular Mechanism of Action.Current medicinal chemistry · 2025Article
- Article
- Role and mechanism of the Dectin-1-mediated Syk/NF-κB signaling pathway inExperimental and therapeutic medicine · 2022Article
- Article
- Similarities and differences in surface receptor expression by THP-1 monocytes and differentiated macrophages polarized using seven different conditioning regimens.Cellular immunology · 2018Article
- Inhibition of miR-155 attenuates abdominal aortic aneurysm in mice by regulating macrophage-mediated inflammation.Bioscience reports · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.