Regulation of alveolar macrophage death in acute lung inflammation

被引：274

作者：

Fan, Erica K. Y. ^{[1
]}

Fan, Jie ^{[2
,3
,4
]}

机构：

[1] Univ Pittsburgh, Kenneth P Dietrich Sch Arts & Sci, Pittsburgh, PA 15260 USA

[2] Univ Pittsburgh, Dept Surg, Sch Med, Pittsburgh, PA 15213 USA

[3] Vet Affairs Pittsburgh Healthcare Syst, Res & Dev, Pittsburgh, PA 15240 USA

[4] Univ Pittsburgh, McGowan Inst Regenerat Med, Pittsburgh, PA 15219 USA

来源：

RESPIRATORY RESEARCH | 2018年 / 19卷

基金：

美国国家卫生研究院;

关键词：

Acute lung injury; Macrophages; Cell death; Pyroptosis; Necroptosis; Autophagy; MIXED LINEAGE KINASE; PROGRAMMED CELL-DEATH; DOMAIN-LIKE PROTEIN; RESPIRATORY-DISTRESS-SYNDROME; MULTIPLE ORGAN FAILURE; ISCHEMIA-REPERFUSION INJURY; HEMORRHAGIC-SHOCK PRIMES; NECROPTOSIS IN-VIVO; SEVERE BLUNT TRAUMA; TLR2; UP-REGULATION;

D O I：

10.1186/s12931-018-0756-5

中图分类号：

R56 [呼吸系及胸部疾病];

学科分类号：

摘要：

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.

引用

页数：13

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