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首页> 外文期刊>Scientific reports. >Neutrophil extracellular traps and monocyte subsets at the culprit lesion site of myocardial infarction patients
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Neutrophil extracellular traps and monocyte subsets at the culprit lesion site of myocardial infarction patients

机译：中性粒细胞细胞外陷阱和单核细胞亚群在心肌梗死患者的罪魁祸首病灶

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Neutrophils release their chromatin into the extracellular space upon activation. These web-like structures are called neutrophil extracellular traps (NETs) and have potent prothrombotic and proinflammatory properties. In ST-elevation myocardial infarction (STEMI), NETs correlate with increased infarct size. The interplay of neutrophils and monocytes impacts cardiac remodeling. Monocyte subsets are classified as classical, intermediate and non-classical monocytes. In the present study, in vitro stimulation with NETs led to an increase of intermediate monocytes and reduced expression of CX3CR1 in all subsets. Intermediate monocytes have been associated with poor outcome, while non-classical CX3CR1-positive monocytes could have reparative function after STEMI. We characterized monocyte subsets and NET markers at the culprit lesion site of STEMI patients (n?=?91). NET surrogate markers were increased and correlated with larger infarct size and with fewer non-classical monocytes. Intermediate and especially non-classical monocytes were increased at the culprit site compared to the femoral site. Low CX3CR1 expression of monocytes correlated with high NET markers and increased infarct size. In this translational system, causality cannot be proven. However, our data suggest that NETs interfere with monocytic differentiation and receptor expression, presumably promoting a subset shift at the culprit lesion site. Reduced monocyte CX3CR1 expression may compromise myocardial salvage.
机译：中性粒细胞在活化时将它们的染色质释放到细胞外空间中。这些类似网状结构称为嗜中性粒细胞细胞外疏水阀（网），并且具有有效的孕激素和促炎特性。在ST升高心肌梗死（Stemi）中，网与梗塞尺寸的增加相关。中性粒细胞和单核细胞的相互作用会影响心脏重塑。单核细胞子集被分类为经典，中间和非古典单核细胞。在本研究中，用网的体外刺激导致中间单核细胞的增加，并在所有子集中减少CX3CR1的表达。中间体单核细胞已与差的结果有关，而非古典CX3CR1阳性单核细胞可能在茎后具有重复函数。我们在STEMI患者的罪魁祸首病变位点（N？= 91）中表征了单核细胞亚群和净标题。净替代标记增加并与较大的梗塞大小和较少的非典型单核细胞相关。与股本位点相比，罪魁祸首位点在罪魁祸首中升高了中间体和特别是非典型的单核细胞。低CX3CR1单核细胞的表达与高净标题相关，梗塞尺寸增加。在此翻译系统中，无法证明因果关系。然而，我们的数据表明净干扰单核细胞分化和受体表达，可能促进罪魁祸首病变部位的次集移位。减少单核细胞CX3CR1表达可能损害心肌挽损。

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