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Early recruited neutrophils promote asthmatic inflammation exacerbation by release of neutrophil elastase.
Cellular Immunology ( IF 3.7 ) Pub Date : 2020-04-03 , DOI: 10.1016/j.cellimm.2020.104101
Qingyu Weng 1 , Chen Zhu 1 , Kua Zheng 1 , Yinfang Wu 1 , Lingling Dong 1 , Yanping Wu 1 , Miao Li 1 , Jiaxin Shen 1 , Songmin Ying 1 , Huahao Shen 1 , Zhihua Chen 1 , Wen Li 1
Affiliation  

Neutrophils can regulate adaptive immune responses and contribute to chronic inflammation including asthma. However, the roles and mechanisms of neutrophils in initiating eosinophilic airway inflammation remain incompletely understood. Neutrophil elastase (NE) is a component of azurophilic granules and a serine protease with potent functions during inflammation. Here, we showed that neutrophils were early recruited at the onset of asthmatic inflammation by related chemokines. Furthermore, neutrophils could capture allergens and release NE to promote neutrophil aggregation at first. Then they prompt eosinophil infiltration and amplify type 2 immune responses in later phases. Also, this process can be rescued by administration of the NE inhibitor (GW311616). Our data collectively indicate that neutrophils could contribute to asthmatic inflammation by releasing NE.

中文翻译:

早期募集的中性粒细胞通过释放中性粒细胞弹性蛋白酶来促进哮喘炎症加重。

中性粒细胞可以调节适应性免疫反应,并导致包括哮喘在内的慢性炎症。然而,中性粒细胞在引发嗜酸性气道炎症中的作用和机制仍未完全了解。中性粒细胞弹性蛋白酶(NE)是嗜酸性颗粒的一种成分,是一种在炎症过程中具有强大功能的丝氨酸蛋白酶。在这里,我们显示嗜中性粒细胞在哮喘炎症发作时由相关趋化因子早期募集。此外,中性粒细胞起初可以捕获过敏原并释放NE以促进中性粒细胞聚集。然后,它们促使嗜酸性粒细胞浸润,并在以后的阶段放大2型免疫应答。而且,可以通过施用NE抑制剂(GW311616)来挽救该过程。
更新日期:2020-04-03
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