ArticleMycopathologia2015
Early transcriptional response of human monocyte-like THP-1 cells in response to Trichosporon asahii infection.
Article in Mycopathologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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
1 citing paper in PubMed, 3 citations in OpenAlex.
- The Cell Biology of theFrontiers in cellular and infection microbiology · 2017Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trichosporon asahii is the major cause of invasive trichosporonosis, but little is known about the host immune response to this pathogen. In this study, the early transcriptional response of human monocyte-like THP-1 cells to T. asahii infection was evaluated using cDNA microarray and 1,315 differentially expressed genes were identified. The up-regulated genes were mostly involved in both innate and adaptive immune responses, as well as apoptosis and anti-apoptosis processes. Genes encoding the pro-inflammatory cytokines TNF-α, IL-1β, IL18 and IL-23α, along with the both C-C motif and C-X-C motif chemokines were strongly up-regulated, suggesting that THP-1 cells can mount a powerful inflammatory response to T. asahii infection. Genes encoding pattern recognition receptors were found up-regulated, such as dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin, cluster of differentiation 36 and the long pentraxin 3. Genes encoding members of the dual-spasticity phosphates family were up-regulated, and these genes were considered as a negative feedback mechanism to prevent excessive inflammatory response. The down-regulated genes in T. asahii-infected THP-1 cells were predominantly associated with cell cycle, mitosis, cell division and DNA repair. Thus, our study defines the early transcriptional response of monocyte-like THP-1 cells to T. asahii infection and provides a foundation for further investigations into the pathogenesis of T. asahii infection.
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Registered trials
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