Interleukin- (IL-) 17 is increased in acute myocardial infarction (AMI) and plays a key role in inflammatory diseases through its involvement in the activation of leukocytes. Here, we describe for the first time the effect of IL-17 in the migration and activation of monocyte subsets in patients during ST-segment elevation myocardial infarction (STEMI) and post-STEMI. We analyzed the circulating levels of IL-17 in patient plasma. A gradual increase in IL-17 was found in STEMI and post-STEMI patients. Additionally, IL-17 had a powerful effect on the recruitment of CD14⁺⁺CD16⁺/CD14⁺CD16⁺⁺ monocytes derived from patients post-STEMI compared with the monocytes from patients with STEMI, suggesting that IL-17 recruits monocytes with inflammatory activity post-STEMI. Furthermore, IL-17 increased the expression of TLR4 on CD14⁺CD16^- and CD14⁺⁺CD16⁺/CD14⁺CD16⁺⁺ monocytes post-STEMI and might enhance the response to danger-associated molecular patterns post-STEMI. Moreover, IL-17 induced secretion of IL-6 from CD14⁺⁺CD16⁻ and CD14⁺⁺CD16⁺/CD14⁺CD16⁺⁺ monocytes both in STEMI and in post-STEMI, which indicates that IL-17 has an effect on the secretion of proinflammatory cytokines from monocytes during STEMI and post-STEMI. Overall, we demonstrate that in STEMI and post-STEMI, IL-17 is increased and induces the migration and activation of monocyte subsets, possibly contributing to the inflammatory response through TLR4 and IL-6 secretion.

中文翻译：

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白细胞介素17在ST段抬高型心肌梗死患者单核细胞亚群激活中的作用。

白细胞介素-（IL-）17在急性心肌梗死（AMI）中增加，并通过参与白细胞活化而在炎症性疾病中发挥关键作用。在这里，我们首次描述了IL-17在ST段抬高型心肌梗塞（STEMI）和STEMI后患者单核细胞亚群的迁移和激活中的作用。我们分析了患者血浆中IL-17的循环水平。在STEMI和STEMI后患者中发现IL-17逐渐升高。此外，IL-17对募集CD14 ⁺⁺ CD16 ⁺ / CD14 ⁺ CD16 ⁺⁺具有强大的作用与来自STEMI患者的单核细胞相比，来自STEMI患者的单核细胞表明IL-17募集具有STEMI后炎症反应的单核细胞。此外，IL-17增加的TLR4对CD14表达⁺ CD16 ^-和CD14 ⁺⁺ CD16 ⁺ / CD14 ⁺ CD16 ⁺⁺单核细胞后的STEMI和可能提高到危险相关的分子模式后的STEMI的响应。此外，从CD14 IL-6的IL-17诱导的分泌⁺⁺ CD16 ^-和CD14 ⁺⁺ CD16 ⁺ / CD14 ⁺ CD16 ⁺⁺STEMI和STEMI后均存在单核细胞，这表明IL-17对STEMI和STEMI后单核细胞分泌促炎细胞因子具有影响。总的来说，我们证明在STEMI和STEMI后，IL-17升高并诱导单核细胞亚群的迁移和激活，可能通过TLR4和IL-6分泌促进炎症反应。