Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, Maryland.
Am J Respir Crit Care Med. 2018 Mar 15;197(6):708-727. doi: 10.1164/rccm.201705-1043SO.
Pseudomonas aeruginosa is a complex gram-negative facultative anaerobe replete with a variety of arsenals to activate, modify, and destroy host defense mechanisms. The microbe is a common cause of nosocomial infections and an antibiotic-resistant priority pathogen. In the lung, P. aeruginosa disrupts upper and lower airway homeostasis by damaging the epithelium and evading innate and adaptive immune responses. The biology of these interactions is essential to understand P. aeruginosa pathogenesis. P. aeruginosa interacts directly with host cells via flagella, pili, lipoproteins, lipopolysaccharides, and the type III secretion system localized in the outer membrane. P. aeruginosa quorum-sensing molecules regulate the release of soluble factors that enhance the spread of infection. These characteristics of P. aeruginosa differentially affect lung epithelial, innate, and adaptive immune cells involved in the production of mediators and the recruitment of additional immune cell subsets. Pathogen interactions with individual host cells and in the context of host acute lung infection are discussed to reveal pathways that may be targeted therapeutically.
铜绿假单胞菌是一种复杂的革兰氏阴性兼性厌氧菌，拥有多种激活、修饰和破坏宿主防御机制的武器。这种微生物是医院获得性感染的常见原因，也是一种对抗生素具有耐药性的优先病原体。在肺部，铜绿假单胞菌通过破坏上皮细胞并逃避先天和适应性免疫反应来破坏上呼吸道和下呼吸道的内稳态。这些相互作用的生物学对于理解铜绿假单胞菌的发病机制至关重要。铜绿假单胞菌通过鞭毛、菌毛、脂蛋白、脂多糖和位于外膜中的 III 型分泌系统直接与宿主细胞相互作用。铜绿假单胞菌群体感应分子调节可溶性因子的释放，这些因子增强了感染的传播。铜绿假单胞菌的这些特性会对参与产生介质和招募更多免疫细胞亚群的肺上皮细胞、先天和适应性免疫细胞产生不同的影响。本文讨论了病原体与单个宿主细胞以及在宿主急性肺感染背景下的相互作用，以揭示可能具有治疗靶向性的途径。
