Dual-species transcriptional profiling during systemic candidiasis reveals organ-specific host-pathogen interactions.
Dual-species transcriptional profiling during systemic candidiasis reveals organ-specific host-pathogen interactions.
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DOI：
10.1038/srep36055
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发表时间：
2016-11-03
影响因子：
4.6
通讯作者：
Jacobsen ID
中科院分区：
文献类型：
--
作者：
Hebecker B;Vlaic S;Conrad T;Bauer M;Brunke S;Kapitan M;Linde J;Hube B;Jacobsen ID
白色念珠菌是危及生命的真菌血液感染的常见原因。在系统性念珠菌病的小鼠模型中，肾脏是主要靶器官，而肝脏和脾脏中的真菌负荷随着时间的推移而下降。为了更好地了解宿主与病原体相互作用中的这些器官特异性差异，我们对小鼠肾脏、肝脏和脾脏进行了基因表达谱分析，并确定了肝脏和肾脏中的真菌转录组。我们观察到转录免疫反应延迟，并伴有肾脏中真菌应激反应基因的延迟诱导。相比之下，肝脏中促炎反应的早期上调与类似于吞噬作用的真菌转录组相关，表明吞噬细胞对肝脏中的真菌控制有显着贡献。值得注意的是，白色念珠菌菌丝相关基因在肝脏中没有可见丝状化的情况下上调，表明该器官中基因表达和形态的解偶联以及菌丝相关基因的形态独立效应。一致地，宿主和病原体转录数据在种间基因调控网络中的整合表明白色念珠菌细胞壁重塑和代谢与器官特异性免疫反应的联系。
Candida albicans is a common cause of life-threatening fungal bloodstream infections. In the murine model of systemic candidiasis, the kidney is the primary target organ while the fungal load declines over time in liver and spleen. To better understand these organ-specific differences in host-pathogen interaction, we performed gene expression profiling of murine kidney, liver and spleen and determined the fungal transcriptome in liver and kidney. We observed a delayed transcriptional immune response accompanied by late induction of fungal stress response genes in the kidneys. In contrast, early upregulation of the proinflammatory response in the liver was associated with a fungal transcriptome resembling response to phagocytosis, suggesting that phagocytes contribute significantly to fungal control in the liver. Notably, C. albicans hypha-associated genes were upregulated in the absence of visible filamentation in the liver, indicating an uncoupling of gene expression and morphology and a morphology-independent effect by hypha-associated genes in this organ. Consistently, integration of host and pathogen transcriptional data in an inter-species gene regulatory network indicated connections of C. albicans cell wall remodelling and metabolism to the organ-specific immune responses.
影响因子：
4.6
作者：
Hebecker B;Vlaic S;Conrad T;Bauer M;Brunke S;Kapitan M;Linde J;Hube B;Jacobsen ID
通讯作者：
Jacobsen ID