FLUCONAZOLE-BIOFILM MATRIX IN CANDIDA ALBICANS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 中心，不一定是研究者的机构。 医疗器械为微生物提供了一个生态位，以附着并繁殖成成熟的粘附生物膜群落。 生物体通常被抗微生物药物和宿主防御所消灭，在生物膜生长期间蓬勃发展。 白念珠菌真菌生物膜中这种显着的抗菌素耐药性的机制仍不清楚。 我们建议在生物膜生长过程中产生的葡聚糖组装形成一个能够螯合抗真菌药物的粘附基质，使细胞抵抗其作用。 这种新的真菌耐药性机制是生物膜特异性的，对病原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.