FLUCONAZOLE-BIOFILM MATRIX IN CANDIDA ALBICANS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 医疗器械为微生物附着和繁殖到成熟的贴壁生物膜群落提供了一个生态位。通常被抗菌药物和宿主防御措施消除的微生物在生物膜生长过程中蓬勃发展。白色念珠菌生物被膜中这种显着的抗菌素耐药性的机制尚不清楚。我们建议在生物膜生长过程中产生的葡聚糖组装成能够隔离抗真菌药物的粘附性基质，使细胞抵抗它们的作用。这种新的真菌耐药机制具有生物被膜特异性，对病原性真菌和医疗器械感染的耐药性研究具有广泛的意义。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Medical devices provide an ecological niche for microbial organisms to attach and propagate into a mature adherent biofilm community. Organisms typically eliminated by antimicrobial drugs and host defenses flourish during biofilm growth. The mechanism of this remarkable antimicrobial resistance in Candida albicans fungal biofilms remains unclear. We propose glucans produced during biofilm growth assemble to form an adhesive matrix capable of sequestering antifungal drugs, rendering cells resistant their action. This novel mechanism of resistance in fungi is biofilm-specific and has broad implications for the study of resistance in pathogenic fungi and medical device infections.