Report of the 'mechanisms of lung injury and immunomodulator interventions in influenza' workshop, 21 March 2010, Ventura, California, USA.
Report of the 'mechanisms of lung injury and immunomodulator interventions in influenza' workshop, 21 March 2010, Ventura, California, USA.
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2010年3月21日，美国加利福尼亚州文图拉（Ventura）的流感工作室中肺损伤和免疫调节剂干预措施的机制的报告。
DOI：
10.1111/j.1750-2659.2011.00278.x
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发表时间：
2011-11
影响因子：
4.4
通讯作者：
Hayden FG
中科院分区：
文献类型：
--
作者：
Howard WA;Peiris M;Hayden FG
请将本文引用为：霍华德等人（2011）“流感中肺损伤和免疫调节剂干预机制”研讨会报告，2010年3月21日，美国加州文图拉 *。流感和其他呼吸道病毒5（6），453-e475。流感的临床病程和肺损伤的程度由病毒和宿主因素决定，有时还包括继发性细菌感染和基础疾病的加重。病毒复制和宿主免疫应答之间的平衡是疾病发病机制的核心，严重流感感染中肺损伤的程度可能部分归因于过度旺盛或失调的先天性炎症应答或有时缺乏应答。急性呼吸窘迫综合征（ARDS）是严重流感相关呼吸衰竭的主要原因。ARDS可由直接肺损伤（例如呼吸道病原体）和全身性损伤（例如脓毒症）触发，并且与感染性或非感染性损伤相关的炎症反应会加剧肺损伤。本次研讨会旨在回顾目前对急性流感肺损伤的认识，并描述流感和其他呼吸道病原体感染常见的肺损伤的细胞和分子机制。此外，靶向宿主反应蛋白和途径的治疗药物被确定，并审查了正在开发的研究药物。一个合乎逻辑的策略是将联合收割机抗病毒治疗与改变过度宿主反应或补充缺陷反应的药物结合起来。然而，更好地理解与流感和其他病原体引起的急性肺损伤相关的常见细胞信号传导途径对于理解肺损伤的免疫病理学原因是必要的。这将有助于确定哪些免疫调节干预可能是有用的，并预测其使用的适当时机和后果。
Please cite this paper as: Howard et al. (2011) Report of the ‘Mechanisms of lung injury and immunomodulator interventions in influenza’ workshop, 21 March 2010, Ventura, California, USA*. Influenza and Other Respiratory Viruses 5(6), 453–e475. The clinical course of influenza and the extent of lung injury are determined by both viral and host factors, as well as sometimes secondary bacterial infections and exacerbations of underlying conditions. The balance between viral replication and the host immune responses is central to disease pathogenesis, and the extent of lung injury in severe influenza infections may be due in part to overly exuberant or dysregulated innate inflammatory responses or sometimes deficient responses. Acute respiratory distress syndrome (ARDS) is the principal cause of respiratory failure associated with severe influenza. ARDS can be triggered by both direct lung insults (e.g. respiratory pathogens) and systemic insults (e.g. sepsis), and the lung damage is exacerbated by the inflammatory response associated with either infectious or non‐infectious insults. This workshop aimed to review the current understanding of lung injury in acute influenza and describe cellular and molecular mechanisms of lung injury that are common to influenza and infections by other respiratory pathogens. In addition, therapeutic agents that target host response proteins and pathways were identified and investigational agents in development reviewed. A logical strategy would be to combine antiviral treatment with drugs that modify excessive host responses or supplement deficient ones. However, a better understanding of common cell signalling pathways associated with acute lung injury caused by influenza and other pathogens is necessary to understand immunopathologic causes of lung injury. This will help determine which immunomodulatory interventions might be useful, and to predict the appropriate timing and consequences of their use.