急性肺损伤/呼吸窘迫综合征（ALI/ARDS）防治的关键在于及早有效阻断肺损伤的发生发展,恢复及维持有效的肺氧合功能。ALI/ARDS救治过程中面临的主要难题是减阻炎症反应和机械通气相关肺损伤(VILI)。虽然小潮气量通气对患者有一定保护作用，但病死率仍居高不下。因而通过联合应用化学和生物方法来消除或抑制炎症反应，可能可以更有效地减轻肺损伤。本团队基于前期对ALI/ARDS致病机理协作研究的基础，拟运用生物芯片与组学技术、多种肺损伤动物模型、动态实时监测流感病毒感染和肺损伤标本生物资源库等，从分子、细胞和整体水平阐释：1）呼吸机相关损伤及肺纤维化关键调控机制；2）牵张导向的肺保护通气策略与模式；3）序贯免疫吸附、抗体治疗以及抑制中性粒细胞多肽HNP受体P2Y6等干预措施；4）预警生物标记物及干预的切入点等，对ALI/ARDS发生发展及转归的影响和机制，取得突破性进展并为临床救治提供依据。

The key to managing acute lung injury/acute respiratory distress syndrome (ALI/ARDS) includes controlling underlying causes, preventing lung injury, recuperating and sustaining oxygenation function effectively. Pulmonary excessive inflammatory response and ventilator-associated lung injury (VILI) are the major problems in clinical treatment for ALI/ARDS. How to reduce ventilation related lung injury is vital. Besides improving pulmonary oxygenation function, it is crucial to eliminate and inhibit excessive release of inflammatory cytokines in lung injury. Based on our earlier studies on pathogenic mechanism and clinical control of ALI/ARDS, our team, jointed by two leading research hospitals in Guangzhou and Beijing, will analyze the role and mechanism of interventions on lung injury at the level of molecular, cellular and whole living subjects, to understand the mechanism of controlling ALI/ARDS by using lung-protective mechanical ventilation, removing pathogen and residual, clearing cytokines and chemokines, and inhibiting neutrophil polypeptides P2Y6 receptor. A number of inflammatory lung injury models in mice, tree shrews, and pigs will be established. Critical and new techniques and instruments such as protein chips, sequential plasma exchange and immunoadsorption (SPEIA), HNP transgenic mice, biological specimen repository of lung injury and a unique luciferase-encoded influenza viruses will be employed in this study. We will explore biological markers and the point of intervention to provide evidence for improving prevention and treatment of ALI/ARDS and for a better outcome upon ALI/ARDS.