The induction and consequences of Influenza A virus-induced cell death.

The induction and consequences of Influenza A virus-induced cell death.
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DOI:
10.1038/s41419-018-1035-6
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发表时间:
2018-09-25
影响因子:
9
通讯作者:
Poon IKH
Poon IKH
中科院分区:
生物学1区
文献类型:
--
作者:
Atkin-Smith GK;Duan M;Chen W;Poon IKH

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甲型流感病毒 (IAV) 感染会导致上呼吸道、下呼吸道和肺实质内的大量细胞死亡。在严重感染中,高水平的细胞死亡会加剧炎症并破坏上皮细胞屏障的完整性,导致呼吸衰竭。气道和肺泡上皮细胞的 IAV 感染促进免疫细胞浸润到肺部,因此巨噬细胞、单核细胞和中性粒细胞等免疫细胞类型很容易暴露于 IAV 并导致感染诱导死亡。尽管IAV感染后通过细胞凋亡和坏死诱导细胞死亡是众所周知的现象,但导致细胞死亡的分子决定因素尚未完全了解。在这里,我们回顾了目前对 IAV 诱导的细胞死亡的理解,并严格评估细胞死亡在帮助恢复肺稳态或 IAV 诱导的肺部病理进展方面的后果。
Infection with Influenza A virus (IAV) causes significant cell death within the upper and lower respiratory tract and lung parenchyma. In severe infections, high levels of cell death can exacerbate inflammation and comprise the integrity of the epithelial cell barrier leading to respiratory failure. IAV infection of airway and alveolar epithelial cells promotes immune cell infiltration into the lung and therefore, immune cell types such as macrophages, monocytes and neutrophils are readily exposed to IAV and infection-induced death. Although the induction of cell death through apoptosis and necrosis following IAV infection is a well-known phenomenon, the molecular determinants responsible for inducing cell death is not fully understood. Here, we review the current understanding of IAV-induced cell death and critically evaluate the consequences of cell death in aiding either the restoration of lung homoeostasis or the progression of IAV-induced lung pathologies.
该植物通过非凋亡的膜液化过程来防御NAD1的NAD1诱导肿瘤细胞死亡。
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