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铜绿假单胞菌和肺炎克雷伯菌对肺部固有免疫清除机制的适应。

Pseudomonas aeruginosa and Klebsiella pneumoniae Adaptation to Innate Immune Clearance Mechanisms in the Lung.

出版信息

J Innate Immun. 2018;10(5-6):442-454. doi: 10.1159/000487515. Epub 2018 Apr 4.

Abstract

Many different species of gram-negative bacteria are associated with infection in the lung, causing exacerbations of chronic obstructive pulmonary disease, cystic fibrosis (CF), and ventilator-associated pneumonias. These airway pathogens must adapt to common host clearance mechanisms that include killing by antimicrobial peptides, antibiotics, oxidative stress, and phagocytosis by leukocytes. Bacterial adaptation to the host is often evident phenotypically, with increased extracellular polysaccharide production characteristic of some biofilm-associated organisms. Given the relatively limited repertoire of bacterial strategies to elude airway defenses, it seems likely that organisms sharing the same ecological niche might also share common strategies to persistently infect the lung. In this review, we will highlight some of the major factors responsible for the adaptation of Pseudomonas aeruginosa to the lung, addressing how growth in biofilms enables persistent infection, relevant to, but not limited to, the pathogenesis of infection in CF. In contrast, we will discuss how carbapenem-resistant Klebsiella pneumoniae evade immune clearance, an organism often associated with ventilator-associated pneumonia and health-care-acquired pneumonias, but not a typical pathogen in CF.

摘要

许多不同种属的革兰氏阴性菌与肺部感染有关,导致慢性阻塞性肺疾病(COPD)、囊性纤维化(CF)和呼吸机相关性肺炎的恶化。这些气道病原体必须适应常见的宿主清除机制,包括抗菌肽、抗生素、氧化应激和白细胞吞噬的杀伤作用。细菌对宿主的适应通常表型明显,一些生物膜相关生物的胞外多糖产生增加是其特征。鉴于细菌逃避气道防御的策略相对有限,似乎具有相同生态位的生物也可能具有共同的策略来持续感染肺部。在这篇综述中,我们将重点介绍导致铜绿假单胞菌适应肺部的一些主要因素,探讨生物膜中的生长如何使持续性感染成为可能,这与 CF 中的感染发病机制有关,但并不局限于此。相比之下,我们将讨论耐碳青霉烯类肺炎克雷伯菌如何逃避免疫清除,这种生物通常与呼吸机相关性肺炎和医院获得性肺炎有关,但不是 CF 的典型病原体。

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