白色念珠菌(Candida albicans)是人體中一種共生的菌類 ，會造成口腔或生殖器官的感染 ，在正常的人體內沒有致病力 ，但是在免疫不全的病患有很高的致死率。因此 ，了解白色念珠菌的致病以及他們和宿主之間的關係非常重要。然而目前為止 ，不同的階段宿主和病原之間的調控網路還不是很清楚。
在這研究中 ，我們建立了白色念珠菌和斑馬魚(zebrafish)之間的動態宿主-病原調控網路(host-pathogen interaction network) ，結合時間序列微陣列(time-series microarray data) ，可以建立三個不同感染階段的調控網路:附著階段(adhesion stage) ，入侵階段(invasion stage) ，破壞階段(damage stage)。由於鐵對於宿主和病原都是不可或缺的 ，在感染過程中他們之間會有競爭鐵的現象 ，因此我們建立了與鐵作用相關的調控網路。此外 ，我們也建立了和葡萄糖相關的調控網路 ，因為葡糖糖已經被確認是和病原的菌絲形成有關 ，而菌絲又有利於病原入侵宿主。根據鐵和葡萄糖作用相關的調控網路 ，我們可以確認在不同的階段哪些基因是有很多連結的節點(hub) ，或是在不同的階段哪些節點的變化是很大的。
根據建立的白色念珠菌和斑馬魚之間的動態調控網路 ，我們可以了解在不同的三個階段關於鐵的競爭和葡萄醣代謝是如何的表現。有趣的是 ，在附著階段 ，和鐵相關的白色念珠菌基因和斑馬魚蛋白質表現非常活躍 ，到了入侵階段 ，換成和葡萄糖相關的白色念珠菌基因和斑馬魚蛋白質表現比較活躍 ，而最後的破壞階段 ，又換成和鐵相關的白色念珠菌基因和斑馬魚蛋白質表現活躍了。

Candida albicans is a commensal diploid fungus that could cause opportunistic oral and genital infections in humans. Though benign for immunocompetent humans, systemic fungal infections of C. albicans have become major causes of morbidity and mortality in immunocompromised patients. As a result, the understanding of the dynamics of C. albicans pathogenesis and its interaction with the host has emerged as an important topic of study. However, relatively little is known about the host-pathogen interaction networks and the corresponding evolution of the networks
across different stages of infection.
In this study, we were able to construct the host-pathogen interaction networks between C. albicans and zebrafish for three different infection stages, i.e., the adhesion, the invasion, and the damage stage. Iron is an essential element for both pathogen and host, and intense competition for this precious metal between host and pathogen often occurs during infection. In addition, glucose has been identified as an important resource during hyphae formation, which is highly related to the invasion of pathogen during infection. So we focused on the construction of the interaction networks associated with iron and glucose. From the two resulting interaction networks, we identified highly connected hub genes that are relevant to iron competition or glucose metabolism during infection; distinguished pertinent genes whose connectivity change significantly from stage to stage; and studied the behaviors of these genes that are differentially regulated during different infection
stages.
The constructed host-pathogen interaction networks for three infection stages provide significant insights into the dynamic regulation for iron competition and glucose metabolism during infection. In fact, based on these interaction networks, we were able to predict the progress of iron competition and glucose metabolism activities throughout the adhesion, invasion, and damage stage. Interestingly, it seems that both C. albicans and zebrafish are more actively involved in the regulation of iron-related genes and proteins during the adhesion stage. During the invasion stage, however, both host and pathogen turn on the regulation of glucose-related genes and proteins. In the last stage of damage, regulatory activities of host and pathogen focus back on iron-related genes and proteins.

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