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关于非典型流感嗜血杆菌在慢性阻塞性肺疾病中持续气道感染的见解

Insights on persistent airway infection by non-typeable Haemophilus influenzae in chronic obstructive pulmonary disease.

作者信息

Ahearn Christian P, Gallo Mary C, Murphy Timothy F

机构信息

Department of Microbiology and Immunology, University at Buffalo, Jacobs School of Medicine and Biomedical Sciences, Buffalo, NY 14203, USA.

Clinical and Translational Research Center, University at Buffalo, Jacobs School of Medicine and Biomedical Sciences, Buffalo, NY 14203, USA.

出版信息

Pathog Dis. 2017 Jun 1;75(4). doi: 10.1093/femspd/ftx042.

Abstract

Non-typeable Haemophilus influenzae (NTHi) is the most common bacterial cause of infection of the lower airways in adults with chronic obstructive pulmonary disease (COPD). Infection of the COPD airways causes acute exacerbations, resulting in substantial morbidity and mortality. NTHi has evolved multiple mechanisms to establish infection in the hostile environment of the COPD airways, allowing the pathogen to persist in the airways for months to years. Persistent infection of the COPD airways contributes to chronic airway inflammation that increases symptoms and accelerates the progressive loss of pulmonary function, which is a hallmark of the disease. Persistence mechanisms of NTHi include the expression of multiple redundant adhesins that mediate binding to host cellular and extracellular matrix components. NTHi evades host immune recognition and clearance by invading host epithelial cells, forming biofilms, altering gene expression and displaying surface antigenic variation. NTHi also binds host serum factors that confer serum resistance. Here we discuss the burden of COPD and the role of NTHi infections in the course of the disease. We provide an overview of NTHi mechanisms of persistence that allow the pathogen to establish a niche in the hostile COPD airways.

摘要

不可分型流感嗜血杆菌(NTHi)是慢性阻塞性肺疾病(COPD)成人患者下呼吸道感染最常见的细菌病因。COPD气道感染会引发急性加重,导致大量发病和死亡。NTHi已进化出多种机制,以便在COPD气道的恶劣环境中建立感染,使病原体能够在气道中持续存在数月至数年。COPD气道的持续感染会导致慢性气道炎症,从而加重症状并加速肺功能的进行性丧失,这是该疾病的一个标志。NTHi的持续存在机制包括表达多种冗余粘附素,这些粘附素介导与宿主细胞和细胞外基质成分的结合。NTHi通过侵入宿主上皮细胞、形成生物膜、改变基因表达和表现出表面抗原变异来逃避宿主免疫识别和清除。NTHi还结合赋予血清抗性的宿主血清因子。在此,我们讨论COPD的负担以及NTHi感染在疾病过程中的作用。我们概述了NTHi持续存在的机制,这些机制使病原体能够在恶劣的COPD气道中建立一个生态位。

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