Institute of Genetic Medicine, Newcastle University Newcastle upon Tyne, UK.
Institute of Genetic Medicine, Newcastle University Newcastle upon Tyne, UK ; Department of Applied Sciences, Faculty of Health & Life Sciences, Northumbria University Newcastle upon Tyne, UK.
Immun Inflamm Dis. 2015 Jun;3(2):56-70. doi: 10.1002/iid3.49. Epub 2015 Mar 1.
CMV infection is responsible for acceleration of immune senescence and linked to systemic pathologies, including cardiovascular diseases. In this study, we investigated differences in the immune response between CMV-seropositive and seronegative patients undergoing primary percutaneous coronary intervention (PPCI) for acute myocardial infarction (MI). Peripheral blood samples were taken at six different time points: pre-, 15, 30, 90 min, 24 h after PPCI and at 3 months after MI. Absolute counts of lymphocyte subpopulations, immune response to specific and nonspecific stimulation, serum cytokines and levels of CMV-IgG, cardiolipin-IgG, and anti-endothelial cell antibodies were assessed. CMV-seropositive patients with MI showed a twofold higher IFN-γ production to PHA-stimulation, up to 2.5-fold higher levels of IP-10 in serum and up to 30% lower serum levels of IL-16 compared to CMV-seronegative individuals. CMV-seropositive patients could be divided into two subgroups with high (IL-10Hi) and low (IL-10Lo) IL-10 serum levels during the acute stage of MI. The IL-10Hi CMV-seropositive subgroup showed an increased exit of late-differentiated T lymphocytes, NK and NKT-like cells from the circulation, which may potentially enhance cytotoxic damage in the ischemic myocardium. Finally, we did not observe an acceleration of autoimmunity by MI in CMV-seropositive individuals. The immune response during acute MI showed characteristic differences between CMV seronegative and seropositive patients, with a stronger pro-inflammatory response in seropositive patients. The effects of IP-10, IL-16, and IL-10 on characteristics of acute immune responses and formation of different immune profiles in CMV-seropositive individuals require further investigation.
巨细胞病毒(CMV)感染是导致免疫衰老加速的原因,并与包括心血管疾病在内的系统性疾病有关。在这项研究中,我们研究了巨细胞病毒血清阳性和血清阴性的急性心肌梗死(MI)患者在接受经皮冠状动脉介入治疗(PPCI)时免疫反应的差异。在六个不同时间点采集外周血样本:PPCI 前、15、30、90 分钟、24 小时后和 MI 后 3 个月。评估淋巴细胞亚群的绝对计数、对特异性和非特异性刺激的免疫反应、血清细胞因子以及 CMV-IgG、心磷脂 IgG 和抗内皮细胞抗体的水平。与 CMV 血清阴性个体相比,CMV 血清阳性 MI 患者对 PHA 刺激的 IFN-γ产生增加了两倍,血清中 IP-10 水平增加了 2.5 倍,血清中 IL-16 水平降低了 30%。CMV 血清阳性患者在 MI 的急性期可分为高(IL-10Hi)和低(IL-10Lo)血清 IL-10 两个亚组。IL-10Hi CMV 血清阳性亚组显示晚期分化 T 淋巴细胞、NK 和 NKT 样细胞从循环中大量流出,这可能潜在增强缺血心肌的细胞毒性损伤。最后,我们没有观察到 MI 在 CMV 血清阳性个体中加速自身免疫。CMV 血清阴性和阳性患者在急性 MI 期间的免疫反应表现出特征性差异,血清阳性患者表现出更强的促炎反应。IP-10、IL-16 和 IL-10 对急性免疫反应特征和 CMV 血清阳性个体中不同免疫谱形成的影响需要进一步研究。