This review guides the reader through the current understanding of the dynamic changes that occur within the cystic fibrosis (CF) lung that allow Pseudomonas aeruginosa to become the dominant pathogen associated with CF. Although recent studies provide some insight, the mechanisms that drive the changing landscape of the lung environment throughout an individual’s lifetime that prime P. aeruginosa to take over and establish chronic infection within the lungs, remain poorly understood. We explore how the CF lung environment shapes the ability of P. aeruginosa to persist in spite of intense antimicrobial therapy. We also highlight the pioneering use of a triple combination cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapy, Trikafta, to restore CFTR function and how it influences P. aeruginosa persistence in the CF lung. We utilize existing data for single modulator therapies to extrapolate the potential future of pathogen infection in the era of Trikafta therapy.

这篇综述将引导读者了解目前对囊性纤维化 (CF) 肺内发生的动态变化的理解，这些变化使铜绿假单胞菌成为与 CF 相关的主要病原体。尽管最近的研究提供了一些见解，但在个体的一生中，促使铜绿假单胞菌接管并在肺部建立慢性感染的肺部环境变化的机制仍然知之甚少。我们探索 CF 肺环境如何塑造铜绿假单胞菌的能力尽管进行了强烈的抗菌治疗，但仍然存在。我们还强调了三重组合囊性纤维化跨膜电导调节剂 (CFTR) 调节剂疗法 Trikafta 的开创性使用，以恢复 CFTR 功能以及它如何影响CF 肺中铜绿假单胞菌的持久性。我们利用现有的单一调节剂疗法数据来推断 Trikafta 疗法时代病原体感染的潜在未来。