Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species.

Could Interleukin-33 (IL-33) Govern the Outcome of an Equine Influenza Virus Infection? Learning from Other Species.
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白细胞介素-33(IL-33)能控制马流感病毒感染的结果吗?向其他物种学习。

DOI:
10.3390/v13122519
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发表时间:
2021-12-15
期刊:
Viruses
影响因子:
--
通讯作者:
Chauché C
Chauché C
中科院分区:
其他
文献类型:
--
作者:
Rozario C;Martínez-Sobrido L;McSorley HJ;Chauché C

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甲型流感病毒(IAV)是马和人类重要的呼吸道病原体。感染者会出现与感染区域气道上皮细胞(AEC)死亡相关的典型呼吸道疾病。IAV毒株的毒力和继发性细菌感染的风险各不相同。IAV非结构蛋白NS 1、PB 1-F2和PA-X是控制AEC死亡和宿主对病毒和细菌感染的免疫应答的重要毒力因子。这些蛋白质的多态性影响其功能。来自人类和小鼠研究的证据表明,在IAV感染后,AEC死亡的方式影响疾病的严重程度。事实上,虽然细胞凋亡被认为是抗炎性的,但坏死被认为会导致肺损伤,并释放损伤相关分子模式(DAMP),如白细胞介素-33(IL-33)。IL-33是由坏死细胞释放的有效炎症介质,在抗病毒和抗细菌免疫中起关键作用。在这里,我们讨论了在人类和小鼠模型中的研究,这些研究调查了病毒决定因素和宿主免疫反应如何控制AEC死亡和随后的肺部IL-33释放,从而影响IAV疾病的严重程度。在马中重现这些数据,并提高我们对IAV感染期间AEC死亡引发的早期免疫反应的理解,将更好地为旨在保护马和人类终身肺部健康的新型治疗或疫苗策略的开发提供信息,遵循One Health方法。
Influenza A viruses (IAVs) are important respiratory pathogens of horses and humans. Infected individuals develop typical respiratory disorders associated with the death of airway epithelial cells (AECs) in infected areas. Virulence and risk of secondary bacterial infections vary among IAV strains. The IAV non-structural proteins, NS1, PB1-F2, and PA-X are important virulence factors controlling AEC death and host immune responses to viral and bacterial infection. Polymorphism in these proteins impacts their function. Evidence from human and mouse studies indicates that upon IAV infection, the manner of AEC death impacts disease severity. Indeed, while apoptosis is considered anti-inflammatory, necrosis is thought to cause pulmonary damage with the release of damage-associated molecular patterns (DAMPs), such as interleukin-33 (IL-33). IL-33 is a potent inflammatory mediator released by necrotic cells, playing a crucial role in anti-viral and anti-bacterial immunity. Here, we discuss studies in human and murine models which investigate how viral determinants and host immune responses control AEC death and subsequent lung IL-33 release, impacting IAV disease severity. Confirming such data in horses and improving our understanding of early immunologic responses initiated by AEC death during IAV infection will better inform the development of novel therapeutic or vaccine strategies designed to protect life-long lung health in horses and humans, following a One Health approach.
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