P2:THE ROLE OF LIPID SIGNALS IN P AERUGINOSA VIRULENCE TOWARDS EPITHELIAL CELLS

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 研究中心，而研究中心不一定是研究者所在的机构。 铜绿假单胞菌是囊性纤维化（CF）患者发病和死亡的最常见原因。来自被铜绿假单胞菌定殖的CF患者的痰液具有可检测水平的30 C12 HSL和已知调节毒力因子的其他分泌的信号分子，并且先前的研究已经发现这些分子中的至少一种30 C12 HSL对宿主细胞造成损伤。铜绿假单胞菌在C.在白色念珠菌中，3 OC 12 HSL浓度比同等浓度的铜绿假单胞菌培养物高8-12倍，我们假设宿主环境可能类似地调节3 OC 12 HSL的产生。本计画的目的是研究绿脓杆菌群体感应分子的产生动力学与宿主效应。

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. Pseudomonas aeruginosa is the most common cause of morbidity and mortality in patients with cystic fibrosis (CF). Sputum from CF patients colonized with P. aeruginosa have detectable levels of 3OC12HSL and other secreted signaling molecules known to regulate virulence factors, and previous studies have found that at least one of these molecules, 3OC12HSL, causes damage to host cells. In P. aeruginosa biofilms on C. albicans, 3OC12HSL concentrations are 8-12 fold higher than in equivalent planktonic P. aeruginosa cultures, we hypothesize that the host environment may similarly regulate 3OC12HSL production. The goal of this project is to examine the production kinetics and host effects of P. aeruginosa quorum sensing molecules.