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首页> 外文期刊>Mycopathologia >Early Transcriptional Response of Human Monocyte-like THP-1 Cells in Response to Trichosporon asahii Infection
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Early Transcriptional Response of Human Monocyte-like THP-1 Cells in Response to Trichosporon asahii Infection

机译:人单核细胞样THP-1细胞对天花粉孢菌感染的早期转录反应。

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摘要

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-alpha, IL-1 beta, IL18 and IL-23 alpha, 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.
机译:Asahii的Trichosporon是造成侵袭性Trichosporonosis的主要原因,但对宿主对该病原体的免疫反应知之甚少。在这项研究中,使用cDNA微阵列评估了人类单核细胞样THP-1细胞对旭状支原体感染的早期转录反应,并鉴定了1315个差异表达基因。上调的基因主要参与先天和适应性免疫应答,以及细胞凋亡和抗凋亡过程。编码促炎性细胞因子TNF-alpha,IL-1 beta,IL18和IL-23 alpha的基因以及CC基序和CXC基序趋化因子均被上调,这表明THP-1细胞可以引起强大的炎症对麻疹沙门氏菌感染的反应。发现编码模式识别受体的基因被上调,例如树突状细胞特异性细胞间粘附分子3捕获非整联蛋白,分化簇36和长五味素3。编码双痉挛性磷酸酯家族成员的基因被上调,这些基因被认为是防止过度炎症反应的负反馈机制。 T. asahii感染的THP-1细胞中下调的基因主要与细胞周期,有丝分裂,细胞分裂和DNA修复有关。因此,我们的研究确定了单核细胞样THP-1细胞对旭状支原体感染的早期转录反应,并为进一步研究旭状支原体感染的发病机理提供了基础。

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