Kenneth P. Dietrich School of Arts & Sciences, University of Pittsburgh, Pittsburgh, PA, 15260, USA.
Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213, USA.
Respir Res. 2018 Mar 27;19(1):50. doi: 10.1186/s12931-018-0756-5.
Acute lung injury (ALI) and its severe form, known as acute respiratory distress syndrome (ARDS), are caused by direct pulmonary insults and indirect systemic inflammatory responses that result from conditions such as sepsis, trauma, and major surgery. The reciprocal influences between pulmonary and systemic inflammation augments the inflammatory process in the lung and promotes the development of ALI. Emerging evidence has revealed that alveolar macrophage (AM) death plays important roles in the progression of lung inflammation through its influence on other immune cell populations in the lung. Cell death and tissue inflammation form a positive feedback cycle, ultimately leading to exaggerated inflammation and development of disease. Pharmacological manipulation of AM death signals may serve as a logical therapeutic strategy for ALI/ARDS. This review will focus on recent advances in the regulation and underlying mechanisms of AM death as well as the influence of AM death on the development of ALI.
急性肺损伤（ALI）及其严重形式，即急性呼吸窘迫综合征（ARDS），是由直接的肺部损伤和来自脓毒症、创伤和大手术等情况的间接全身炎症反应引起的。肺和全身炎症之间的相互影响增强了肺部的炎症过程，并促进了 ALI 的发展。新出现的证据表明，肺泡巨噬细胞（AM）死亡通过影响肺部的其他免疫细胞群，在肺炎症的进展中发挥重要作用。细胞死亡和组织炎症形成正反馈循环，最终导致炎症加剧和疾病发展。对 AM 死亡信号的药理学干预可能是 ALI/ARDS 的一种合理的治疗策略。本综述将重点介绍 AM 死亡的调控和潜在机制的最新进展，以及 AM 死亡对 ALI 发展的影响。
