Platelet Mediated Inflammation in Coronary Artery Disease with Type 2 Diabetes Patients.
Platelet Mediated Inflammation in Coronary Artery Disease with Type 2 Diabetes Patients.
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DOI：
10.2147/jir.s326716
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发表时间：
2021
影响因子：
4.5
通讯作者：
Adela R
中科院分区：
文献类型：
--
作者：
Johny E;Bhaskar P;Alam MJ;Kuladhipati I;Das R;Adela R
2 型糖尿病 (T2DM) 是动脉粥样硬化性冠状动脉疾病发展的公认危险因素。血小板过度活跃和炎症与 T2DM 患者冠状动脉疾病 (CAD) 的发生有关。我们研究了 T2DM_CAD 患者的免疫细胞状态、血小板活化以及血小板-免疫细胞相互作用。研究人群由四组受试者组成：健康对照（CT，n = 20）、T2DM（n = 44）、CAD（n = 20）和T2DM_CAD（n = 38）。通过流式细胞术分析血小板活化、免疫组分析和血小板-免疫细胞相互作用。使用多重测定评估炎性细胞因子/趋化因子的循环水平。与对照组和 CAD 组相比，在 T2DM 和 T2DM_CAD 组中观察到血小板活化增加和血小板免疫细胞聚集体形成增加 (p < 0.05)。我们的免疫组谱分析显示，与对照组相比，T2DM、CAD 和 T2DM_CAD 组的单核细胞亚群和树突状细胞群发生了改变 (p < 0.05)。此外，与对照组相比，T2DM_CAD组中IL-1β、IL-2、IL-4、IL-6、IL-8、IL12p70、IL-13、IL-18、CCL2显着升高，CXCL1、CCL5水平显着降低。我们的离体研究观察到，D-葡萄糖暴露后，血小板-单核细胞聚集体形成增加，且呈时间和浓度依赖性。我们的数据表明 T2DM、CAD 和 T2DM_CAD 与免疫细胞群的改变有关。此外，已证实高血糖会诱导血小板活化并形成血小板免疫细胞聚集，从而可能导致炎症细胞因子和趋化因子的释放，并导致CAD和2型糖尿病的复杂性。
Type 2 diabetes mellitus (T2DM) is a well-established risk factor for the development of atherosclerotic coronary artery disease. Platelet hyperactivity and inflammation are associated with the development of coronary artery disease (CAD) in T2DM patients. We investigated the status of immune cells, platelet activation, and platelet-immune cell interactions in T2DM_CAD patients. The study population consisted of four groups of subjects, healthy control (CT, n = 20), T2DM (n = 44), CAD (n = 20) and T2DM_CAD (n = 38). Platelet activation, immunome profiling and platelet-immune cell interactions were analysed by flow cytometry. The circulatory levels of inflammatory cytokines/chemokines were assessed using multiplex assay. Increased platelet activation and increased platelet-immune cell aggregate formation were observed in T2DM and T2DM_CAD groups compared to the control and CAD groups (p < 0.05). Our immunome profile analysis revealed, altered monocyte subpopulations and dendritic cell populations in T2DM, CAD and T2DM_CAD groups compared to the control group (p < 0.05). Furthermore, significantly increased IL-1β, IL-2, IL-4, IL-6, IL-8, IL12p70, IL-13 IL-18, CCL2, and decreased CXCL1, CCL5 levels were observed in T2DM_CAD group compared to the control group. Our ex-vivo study increased platelet-monocyte aggregate formation was observed upon D-glucose exposure in a time and concentration dependent manner. Our data suggests that T2DM, CAD and T2DM_CAD are associated with altered immune cell populations. Furthermore, it has been confirmed that hyperglycemia induces platelet activation and forms platelet-immune cell aggregation which may lead to the release of inflammatory cytokines and chemokines and contribute to the complexity of CAD and type 2 diabetes.