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首页> 外文期刊>Basic Research in Cardiology >Expression of IL-17A in human atherosclerotic lesions is associated with increased inflammation and plaque vulnerability
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Expression of IL-17A in human atherosclerotic lesions is associated with increased inflammation and plaque vulnerability

机译：IL-17A在人类动脉粥样硬化病变中的表达与炎症增加和斑块易损性有关

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A chronic (auto)immune response is the critical mechanism in atherosclerosis. Interleukin-17A is a pivotal effector cytokine, which modulates immune cell trafficking and initiates inflammation in (auto)immune and infectious diseases. However, expression of IL-17A in the context of human atherosclerosis has hardly been explored. Carotid artery plaques were collected from 79 patients undergoing endarterectomy. Patients were grouped according to their symptomatic status (TIA, stroke), plaque morphology and medication. Quantitative RT-PCR was used to analyze tissue inflammation and immunohistochemistry to assess cellular source of IL-17A expression and lesion morphology. Carotid plaques from patients with ischemic symptoms were characterized by a highly activated inflammatory milieu including accumulation of T cells (p = 0.04) and expression of IL-6 and VCAM1 (p = 0.02, 0.01). Expression of IL-17A and its positive regulators IL-21 and IL-23 was present in atherosclerotic lesions, significantly upregulated in atheromas of symptomatic patients (p = 0.005, 0.004, 0.03), and expression of IL-17A and IL-21 showed a strong correlation (p = 0.002, r = 0.52). The cellular sources of lesional IL-17A expression are T cells, macrophages, B cells and plasma cells. Vulnerable/ruptured (complicated) plaques were significantly associated with IL-17A expression levels (p = 0.003). In addition, IL-17A showed a marked negative correlation with the potent anti-inflammatory/atheroprotective cytokine IL-10 (p = 0.0006, r = −0.46). Furthermore, treatment with a HMG-CoA reductase inhibitor or acetylsalicylic acid showed reduced levels of IL-21, IL-23 and VCAM1 (all p < 0.05), but did not influence IL-17A. The association of IL-17A with ischemic symptoms and vulnerable plaque characteristics suggests that the pro-inflammatory cytokine IL-17A may contribute to atherosclerosis und plaque instability.
机译：慢性（自身）免疫应答是动脉粥样硬化的关键机制。白介素-17A是关键的效应细胞因子，可调节免疫细胞的运输并引发（自身）免疫和感染性疾病的炎症。然而，几乎没有研究在人动脉粥样硬化的情况下IL-17A的表达。从79例接受动脉内膜切除术的患者中收集颈动脉斑块。根据患者的症状状态（TIA，中风），斑块形态和用药分组。定量RT-PCR用于分析组织炎症和免疫组织化学，以评估IL-17A表达的细胞来源和病变形态。患有缺血症状的患者的颈动脉斑块的特征是高度活化的炎症环境，包括T细胞积聚（p = 0.04）以及IL-6和VCAM1的表达（p = 0.02，0.01）。 IL-17A及其阳性调节剂IL-21和IL-23的表达存在于动脉粥样硬化病变中，在有症状患者的动脉粥样硬化中明显上调（p = 0.005、0.004、0.03），并且显示IL-17A和IL-21的表达相关性强（p = 0.002，r = 0.52）。病灶IL-17A表达的细胞来源是T细胞，巨噬细胞，B细胞和浆细胞。易损/破裂（复杂）的斑块与IL-17A表达水平显着相关（p = 0.003）。此外，IL-17A与有效的抗炎/抗动脉粥样硬化细胞因子IL-10呈显着负相关（p = 0.0006，r = -0.46）。此外，用HMG-CoA还原酶抑制剂或乙酰水杨酸治疗可降低IL-21，IL-23和VCAM1的水平（均p <0.05），但不影响IL-17A。 IL-17A与缺血性症状和易损斑块特征的关联表明促炎性细胞因子IL-17A可能导致动脉粥样硬化和斑块不稳定。

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