Centre International de Recherche en Infectiologie, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS de Lyon, 69007 Lyon, France.
Institut des Agents Infectieux, Hospices Civils de Lyon, 69002 Lyon, France.
Int J Mol Sci. 2023 Apr 1;24(7):6609. doi: 10.3390/ijms24076609.
Cystic fibrosis (CF) is a serious genetic disease that leads to premature death, mainly due to impaired lung function. CF lungs are characterized by ongoing inflammation, impaired immune response, and chronic bacterial colonization. (SA) and (PA) are the two most predominant bacterial agents of these chronic infections. Both can colonize the lungs for years by developing host adaptation strategies. In this review, we examined the mechanisms by which SA and PA adapt to the host immune response. They are able to bypass the physical integrity of airway epithelia, evade recognition, and then modulate host immune cell proliferation. They also modulate the immune response by regulating cytokine production and by counteracting the activity of neutrophils and other immune cells. Inhibition of the immune response benefits not only the species that implements them but also other species present, and we therefore discuss how these mechanisms can promote the establishment of coinfections in CF lungs.
囊性纤维化（CF）是一种严重的遗传疾病，主要导致肺功能受损，从而导致过早死亡。CF 肺部的特征是持续的炎症、受损的免疫反应和慢性细菌定植。金黄色葡萄球菌（SA）和铜绿假单胞菌（PA）是这些慢性感染的两种最主要的细菌病原体。这两种病原体都可以通过宿主适应策略在肺部定植多年。在这篇综述中，我们研究了 SA 和 PA 适应宿主免疫反应的机制。它们能够绕过气道上皮细胞的物理完整性，逃避识别，然后调节宿主免疫细胞的增殖。它们还通过调节细胞因子的产生和中和中性粒细胞和其他免疫细胞的活性来调节免疫反应。抑制免疫反应不仅有利于实施这些机制的物种，也有利于其他共存的物种，因此我们讨论了这些机制如何促进 CF 肺部合并感染的建立。
