Department of Oral Biology, School of Dental Medicine, The State University of New York at Buffalo, Buffalo, New York, United States of America.
PLoS Pathog. 2018 Sep 25;14(9):e1007316. doi: 10.1371/journal.ppat.1007316. eCollection 2018 Sep.
Candida albicans is an opportunistic fungal pathogen that can infect oral mucosal surfaces while being under continuous flow from saliva. Under specific conditions, C. albicans will form microcolonies that more closely resemble the biofilms formed in vivo than standard in vitro biofilm models. However, very little is known about these microcolonies, particularly genomic differences between these specialized biofilm structures and the traditional in vitro biofilms. In this study, we used a novel flow system, in which C. albicans spontaneously forms microcolonies, to further characterize the architecture of fungal microcolonies and their genomics compared to non-microcolony conditions. Fungal microcolonies arose from radially branching filamentous hyphae that increasingly intertwined with one another to form extremely dense biofilms, and closely resembled the architecture of in vivo oropharyngeal candidiasis. We identified 20 core microcolony genes that were differentially regulated in flow-induced microcolonies using RNA-seq. These genes included HWP1, ECE1, IHD1, PLB1, HYR1, PGA10, and SAP5. A predictive algorithm was utilized to identify ten transcriptional regulators potentially involved in microcolony formation. Of these transcription factors, we found that Rob1, Ndt80, Sfl1 and Sfl2, played a key role in microcolony formation under both flow and static conditions and to epithelial surfaces. Expression of core microcolony genes were highly up-regulated in Δsfl1 cells and down-regulated in both Δsfl2 and Δrob1 strains. Microcolonies formed on oral epithelium using C. albicans Δsfl1, Δsfl2 and Δrob1 deletion strains all had altered adhesion, invasion and cytotoxicity. Furthermore, epithelial cells infected with deletion mutants had reduced (SFL2, NDT80, and ROB1) or enhanced (SFL2) immune responses, evidenced by phosphorylation of MKP1 and c-Fos activation, key signal transducers in the hyphal invasion response. This profile of microcolony transcriptional regulators more closely reflects Sfl1 and Sfl2 hyphal regulatory networks than static biofilm regulatory networks, suggesting that microcolonies are a specialized pathogenic form of biofilm.
白色念珠菌是一种机会性真菌病原体,在持续受到唾液流动的情况下,能够感染口腔黏膜表面。在特定条件下,白色念珠菌会形成微菌落,这些微菌落比标准的体外生物膜模型更接近体内形成的生物膜。然而,人们对这些微菌落知之甚少,特别是这些专门的生物膜结构与传统的体外生物膜之间的基因组差异。在这项研究中,我们使用了一种新的流动系统,其中白色念珠菌会自发形成微菌落,以进一步描述真菌微菌落的结构及其与非微菌落条件下的基因组学特征。真菌微菌落由放射状分支丝状菌丝组成,这些菌丝相互缠绕,形成极其密集的生物膜,与体内口咽念珠菌感染的结构非常相似。我们使用 RNA-seq 鉴定了 20 个核心微菌落基因,这些基因在流动诱导的微菌落中存在差异表达。这些基因包括 HWP1、ECE1、IHD1、PLB1、HYR1、PGA10 和 SAP5。我们利用预测算法鉴定了十个可能参与微菌落形成的转录因子。在这些转录因子中,我们发现 Rob1、Ndt80、Sfl1 和 Sfl2 在流动和静态条件下以及在与上皮表面的相互作用中,对微菌落的形成起着关键作用。核心微菌落基因的表达在Δsfl1 细胞中高度上调,在Δsfl2 和Δrob1 菌株中下调。使用白色念珠菌Δsfl1、Δsfl2 和Δrob1 缺失株在口腔上皮上形成的微菌落,其粘附、侵袭和细胞毒性均发生改变。此外,感染缺失突变体的上皮细胞的免疫反应降低(SFL2、NDT80 和 ROB1)或增强(SFL2),这表现为丝裂原激活蛋白激酶磷酸化和 c-Fos 激活,这是菌丝侵入反应中的关键信号转导物。这种微菌落转录因子的模式更接近 Sfl1 和 Sfl2 丝状调控网络,而不是静态生物膜调控网络,这表明微菌落是一种特殊的致病性生物膜形式。