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Regulatory T Cells Protect Fine Particulate Matter-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

机译:调节性T细胞保护人脐静脉内皮细胞中细颗粒物诱导的炎症反应。

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摘要

Objective. To investigate the role of CD4+CD25+ T cells (Tregs) in protecting fine particulate matter (PM-) induced inflammatory responses, and its potential mechanisms. Methods. Human umbilical vein endothelial cells (HUVECs) were treated with graded concentrations (2, 5, 10, 20, and 40 µg/cm2) of suspension of fine particles for 24h. For coculture experiment, HUVECs were incubated alone, with CD4+CD25 T cells (Teff), or with Tregs in the presence of anti-CD3 monoclonal antibodies for 48 hours, and then were stimulated with or without suspension of fine particles for 24 hours. The expression of adhesion molecules and inflammatory cytokines was examined. Results. Adhesion molecules, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), and inflammatory cytokines, such as interleukin (IL-) 6 and IL-8, were increased in a concentration-dependent manner. Moreover, the adhesion of human acute monocytic leukemia cells (THP-1) to endothelial cells was increased and NF-κB activity was upregulated in HUVECs after treatment with fine particles. However, after Tregs treatment, fine particles-induced inflammatory responses and NF-κB activation were significantly alleviated. Transwell experiments showed that Treg-mediated suppression of HUVECs inflammatory responses impaired by fine particles required cell contact and soluble factors. Conclusions. Tregs could attenuate fine particles-induced inflammatory responses and NF-κB activation in HUVECs.
机译:目的。目的探讨CD4 + CD25 + T细胞(Tregs)在保护细颗粒物(PM-)诱导的炎症反应中的作用及其潜在机制。方法。用浓度分别为2、5、10、20和40μµg / cm 2 的细颗粒悬浮液处理人脐静脉内皮细胞(HUVEC)24小时。对于共培养实验,将HUVEC与CD4 + CD25 - T细胞(Teff)或与Tregs在抗CD3单克隆抗体存在下单独孵育48小时,然后在有或没有悬浮微粒的情况下刺激24小时。检查粘附分子和炎性细胞因子的表达。结果。包括血管细胞黏附分子1(VCAM-1)和细胞间黏附分子1(ICAM-1)在内的黏附分子以及诸如白介素(IL-)6和IL-8等炎性细胞因子的浓度增加-依赖方式。此外,用细颗粒处理后,HUVECs中的人急性单核细胞白血病细胞(THP-1)与内皮细胞的粘附增加,NF-κB活性上调。然而,在Tregs治疗后,细颗粒诱导的炎症反应和NF-κB活化被显着减轻。 Transwell实验表明,Treg介导的HUVECs炎症反应抑制作用受细颗粒损害需要细胞接触和可溶性因子。结论。 Tregs可以减弱HUVEC中细颗粒诱导的炎症反应和NF-κB活化。

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