胰腺炎与肺部疾病的关系

Michael L Steer
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引用次数: 67

摘要

急性胰腺炎患者可发生急性肺损伤,临床表现为成人呼吸窘迫综合征。大多数在严重急性胰腺炎早期死亡的患者要么死于这种肺损伤,要么死于这种肺损伤。为了探索急性胰腺炎与肺损伤之间的联系,作者的实验室最近进行了一系列研究,使用了多种实验模型和干预措施,包括基因靶向删除趋化因子、细胞因子、特异性受体和粘附分子。这些研究表明,黏附分子如细胞内黏附分子-1 (ICAM-1)、中性粒细胞、血小板活化因子(PAF)、P物质以及通过CCR-1趋化因子受体作用的趋化因子在胰腺炎和肺损伤中具有促炎作用,而补体因子C5a具有抗炎作用。未来的研究将建立在这些观察结果的基础上,扩大促炎和抗炎偶联因子的列表,并探索它们在急性胰腺炎中引起或预防肺损伤的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Relationship between pancreatitis and lung diseases

Patients with acute pancreatitis may develop acute lung injury, manifest clinically as the adult respiratory distress syndrome. Most patients who die during the early stages of severe acute pancreatitis die either with or as a result of this lung injury. To explore the events which couple acute pancreatitis to lung injury, a number of recent studies have been performed in the author's laboratory using a variety of experimental models and interventions including gene-targeted deletion of chemokines, cytokines, specific receptors, and adhesion molecules. These studies have indicated that adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), neutrophils, platelet activating factor (PAF), substance P, and chemokines acting via the CCR-1 chemokine receptor play a pro-inflammatory role while complement factor C5a plays an anti-inflammatory role in pancreatitis and lung injury. Future studies will build on these observations to expand the list of pro- and anti-inflammatory coupling factors and explore the mechanisms by which they act to cause or prevent lung injury in acute pancreatitis.

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