肺部急性炎症的消退。
Resolution of acute inflammation in the lung.
机构信息
Pulmonary and Critical Care Medicine, Department of Internal Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115; email:
出版信息
Annu Rev Physiol. 2014;76:467-92. doi: 10.1146/annurev-physiol-021113-170408. Epub 2013 Dec 2.
Abstract
Acute inflammation in the lung is essential to health. So too is its resolution. In response to invading microbes, noxious stimuli, or tissue injury, an acute inflammatory response is mounted to protect the host. To limit inflammation and prevent collateral injury of healthy, uninvolved tissue, the lung orchestrates the formation of specialized proresolving mediators, specifically lipoxins, resolvins, protectins, and maresins. These immunoresolvents are agonists for resolution that interact with specific receptors on leukocytes and structural cells to blunt further inflammation and promote catabasis. This process appears to be defective in several common lung diseases that are characterized by excess or chronic inflammation. Here, we review the molecular and cellular effectors of resolution of acute inflammation in the lung.
摘要
肺部的急性炎症对于健康至关重要。其消退也是如此。为了应对入侵的微生物、有害刺激物或组织损伤，会引发急性炎症反应来保护宿主。为了限制炎症并防止健康的未受影响的组织受到牵连性损伤，肺部会协调形成专门的促解决介质，特别是脂氧素、解析素、保护素和maresins。这些免疫调节剂是炎症消退的激动剂，与白细胞和结构细胞上的特定受体相互作用，以减弱进一步的炎症并促进衰退。这一过程似乎在几种常见的肺部疾病中存在缺陷，这些疾病的特征是过度或慢性炎症。在这里，我们回顾了肺部急性炎症消退的分子和细胞效应物。
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