Mucus plugging in allergic bronchopulmonary aspergillosis: Implication of the eosinophil DNA traps

Mucus plugging in allergic bronchopulmonary aspergillosis: Implication of the eosinophil DNA traps
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过敏性支气管肺曲霉病中的粘液堵塞:嗜酸性粒细胞 DNA 陷阱的意义

DOI:
10.1016/j.alit.2017.08.002
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发表时间:
2018
影响因子:
6.8
通讯作者:
Hirokawa Makoto
Hirokawa Makoto
中科院分区:
医学2区
文献类型:
--
作者:
Omokawa Ayumi;Ueki Shigeharu;Kikuchi Yuta;Takeda Masahide;Asano Mariko;Sato Kazuhiro;Sano Masaaki;Ito Hiroshi;Hirokawa Makoto

文献摘要

相似文献

变应性支气管肺曲霉病(ABPA)是一种由对曲霉属(即烟曲霉)过度过敏引起的肺部疾病。其特征是哮喘控制不佳,反复肺浸润,支气管扩张,常伴有粘稠的嗜酸性粘液堵塞。[1]尽管对这种高密度粘液产生的机制知之甚少,但这种粘液堵塞的严重程度(可能代表严重炎症)与复发有关。2细胞外陷阱细胞死亡(extracellular trap cell death,ETosis)是人类白细胞,特别是中性粒细胞和嗜酸性粒细胞的一种独特的程序性细胞死亡途径。3与细胞凋亡相反,其特征在于丝状染色质结构(DNA陷阱)的释放。4 DNA陷阱形成被认为是诱捕微生物的先天免疫反应,尽管其过量产生可能是致病的。5例如,在囊性纤维化患者的粘稠气道液体中,存在大量嗜中性粒细胞衍生的DNA陷阱(也称为中性粒细胞胞外陷阱; NET)。4,5值得注意的是,通过吸入重组人DNA酶的治疗改善了肺功能,6表明NET的致病性。
Allergic bronchopulmonary aspergillosis (ABPA) is a pulmonary disorder caused by exaggerated hypersensitivity to Aspergillus species, namely Aspergillus fumigatus. It is characterized by poorly controlled asthma, recurrent pulmonary infiltrates, and bronchiectasis often with thick, viscous eosinophilic mucus plugging. 1 Although the mechanism of this hyperdense mucus generation is poorly understood, the severity of this mucus plugging, which may represent severe inflammation, is associated with recurrent relapse. 2Extracellular trap cell death (ETosis) of human leucocytes, particularly neutrophils and eosinophils, is a distinct programmed cell death pathway. 3 It is characterized by release of filamentous chromatin structures (DNA traps) in contrast to cell apoptosis. 4 DNA trap formation is considered to be an innate immune reaction by ensnaring microorganisms, although its excess production could be pathogenic. 5 For instance, in thick and viscous airway fluids from patients with cystic fibrosis, large numbers neutrophil-derived DNA traps are present (also called neutrophil extracellular traps; NETs). 4, 5 Notably, treatment by inhalation of recombinant human DNase improved lung function, 6 indicating the pathogenicity of NETs.