Inflammasomes are multi-protein complexes tasked with sensing endogenous or exogenous inflammatory signals, and integrating this signal into a downstream response. Inflammasome activation has been implicated in a variety of pulmonary diseases, including pulmonary hypertension, bacterial pneumonia, COPD and asthma. Of increasing interest is the contribution of inflammasome activation in the context of acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Inflammasome activation in both the lung parenchyma and resident immune cells generates intereukin-1β (IL-1β) and IL-18, both of which drive the cascade of lung inflammation forward. Blockade of these responses has been shown to be beneficial in animal models, and is a focus of translational research in the field. In this review, we will discuss the assembly and regulation of inflammasomes during lung inflammation, highlighting therapeutically-viable effector steps. We will examine the importance of IL-1β and IL-18, two key products of inflammasome activation, in ALI, as well as the contribution of the pulmonary endothelial cell to this process. Finally, we will explore translational research moving toward anti-inflammasome therapies for ALI/ARDS, and speculate toward future directions for the field.

中文翻译：

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急性肺损伤中的炎性体激活。

炎性小体是负责感知内源性或外源性炎症信号并将该信号整合到下游反应中的多蛋白复合物。炎性体激活与多种肺部疾病有关，包括肺动脉高压，细菌性肺炎，COPD和哮喘。在急性肺损伤/急性呼吸窘迫综合征（ALI / ARDS）的背景下，炎性体激活的作用越来越引起人们的关注。肺实质和常驻免疫细胞中的炎性体激活均产生白细胞介素-1β（IL-1β）和IL-18，两者均推动肺炎的级联向前发展。这些反应的阻断在动物模型中已被证明是有益的，并且是该领域转化研究的重点。在这篇评论中 我们将讨论在肺部炎症过程中炎症小体的组装和调节，重点介绍在治疗上可行的效应器步骤。我们将检查ALI中炎症小体激活的两个关键产物IL-1β和IL-18的重要性，以及肺内皮细胞对此过程的贡献。最后，我们将探索针对ALI / ARDS的抗炎性疗法的转化研究，并推测该领域的未来方向。