NLRP3炎性体与中性粒细胞在心肌缺血/再灌注损伤中的交流

炎性体是识别危险模式或病原模式的信号平台,炎性体主要分为2大类:点头样受体(NLR)家族和PYHIN家族。炎性体与多种疾病有关,包括各种感染性疾病、炎症性疾病以及缺血再灌注损伤(ischemia reperfusion injury,IRI)等。炎性体与心肌缺血再灌注损伤是目前的研究热点之一。中性粒细胞作为数量最多的骨髓源性细胞,在无菌性炎症及固有免疫传导通路中发挥着重要作用。在缺血再灌注损伤过程中,死亡的心肌细胞释放大量促炎介质,导致炎性体的活化以及中性粒细胞的聚集。我们综述了NLRP3炎症小体在心肌缺血再灌注损伤中的作用,以及在此病理生理过程中NLRP3与中性粒细胞间的信息交流。

The Crosstalk between NLRP3 and Neutrophils during Ischemia Reperfusion Injury

Inflammasomes are platforms recognizing danger-associated molecular pattern (DAMPs) and pathogen-associated molecular pattern (PAMPs), which include NLR family and PYHIN family. Inflammasome was associated with a lot of disease such as infection, acute inflammation and ischemia reperfusion injury (IRI), and the latter was one of the red-hot topics in recent years. Neutrophils, which are a type of polymorphonuclear leukocyte, are well recognized as one of the major players in acute inflammation and innate immune sensing pathways. Adenosine triphosphater (ATP) and some other molecules released from the dead myocardial cells activated the NLRP3 inflammasome to generate an inflammatory microenvironment that attracted circulating neutrophils to adhere within myocardial cells. Here, we review the functions of the NLRP3 inflammasome during myocardial IRI and discuss the crosstalk between NLRP3 and neutrophils during this pathophysiologic process.