[单核细胞亚群分布及其表面CD31强度与肾综合征出血热病程和严重程度相关]。

Xiaozhou Jia, Chunmei Zhang, Fenglan Wang, Yanping Li, Ying Ma, Yusi Zhang, Kang Tang, Ran Zhuang, Yun Zhang, Yan Zhang
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引用次数: 0

摘要

目的探讨肾综合征出血热(HFRS)患者病程、严重程度与单核细胞亚群分布及表面CD31强度的关系。方法采集29例HFRS患者和13例正常人的外周血标本。采用多重免疫荧光染色和流式细胞术检测经典单核细胞亚群(CD14++CD16-)、中介单核细胞亚群(CD14++CD16+)和非经典单核细胞亚群(CD14+CD16++)的动态变化以及CD31对单核细胞亚群的平均荧光强度(MFI)。结果急性期与恢复期和正常对照相比,经典单核细胞亚群占总单核细胞的比例显著降低。恢复期仍远低于正常对照组。与正常对照组相比,HFRS患者经典单核细胞亚群与总单核细胞的比例下降,而重度/危重组与轻度/中度组之间无差异。相反,与恢复期和正常对照相比,急性期HFRS中间单核细胞亚群占总单核细胞的比例显著增加。与正常对照组相比,HFRS患者中间单核细胞亚群与总单核细胞的比例增加,而重度/危重组与轻度/中度组之间无差异。分期或严重程度组在非经典单核细胞亚群与总单核细胞的比例上没有差异。此外,在11例配对样本的HFRS患者中,经典单核细胞亚群的比例呈下降趋势,而中间单核细胞亚群的比例在急性期和恢复期均呈上升趋势。此外,在HFRS急性期,CD31在3个单核细胞亚群上的平均荧光强度(MFI)均下降,其中经典单核细胞亚群CD31的平均荧光强度最高,而正常对照的非经典单核细胞亚群CD31的平均荧光强度最高。恢复期,CD31在经典和中介单核细胞亚群上的MFI均低于正常对照组,而CD31在非经典单核细胞亚群上的MFI仍显著低于正常对照组。最后,重度/危重组CD31在经典和中度单核细胞亚群上的MFI均低于轻度/中度组,不同疾病严重程度组间CD31在非经典单核细胞亚群上的MFI无统计学差异。结论经典和中间型单核细胞亚群占总单核细胞的比例与HFRS病程相关,这些单核细胞亚群表面CD31的表达强度与病程及严重程度相关。然而,CD31在非经典单核细胞亚群上的表面强度仅与疾病的病程相关。总之,在HFRS患者中观察到的单核细胞亚群变化的潜在机制应该进一步研究。
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[Distribution of monocyte subsets and their surface CD31 intensity are associated with disease course and severity of hemorrhagic fever with renal syndrome].

Objective To investigate the relationship between disease courses and severity and monocyte subsets distribution and surface CD31 intensity in patients of hemorrhagic fever with renal syndrome (HFRS). Methods Peripheral blood samples from 29 HFRS patients and 13 normal controls were collected. The dynamic changes of classical monocyte subsets (CD14++CD16-), intermediated monocyte subsets (CD14++CD16+) and non-classical monocyte subsets (CD14+CD16++) and the mean fluorescent intensity (MFI) of CD31 on monocyte subsets were detected by multiple-immunofluorescent staining and flow cytometry. Results In acute phase of HFRS, the ratio of classical monocyte subsets to total monocytes was dramatically decreased compared to convalescent phase and normal control. It was still much lower in convalescent phase compared to normal controls. The ratio of classical monocyte subsets to total monocytes were decreased in HFRS patients compared to that in normal control, whereas there was no difference between severe/critical groups and mild/moderate groups. On the contrary, the ratio of intermediate monocyte subsets to total monocytes in acute phase of HFRS was significantly increased compared to convalescent phase and normal control. The ratio of intermediate monocyte subsets to total monocytes were increased in HFRS patients compared to that in normal control, whereas no difference was found between severe/critical groups and mild/moderate groups. Phases or severity groups had no difference in ratio of non-classical monocyte subsets to total monocytes. Additionally, the ratio of classical monocyte subsets had a tendency to decline and that of intermediate monocyte subsets showed an increase both to total monocytes between the acute and convalescent phases in 11 HFRS patients with paired-samples. Moreover, in acute phase of HFRS, the mean fluorescent intensity (MFI) of CD31 on three monocyte subsets all decreased, specifically classical monocyte subsets showed the highest MFI of CD31 while the normal control reported the highest MFI of CD31 in non-classical monocyte subsets. In convalescent phase, the MFI of CD31 on classical and intermediated monocyte subsets were both lower than that of normal control, while MFI of CD31 was still significantly lower than normal control on non-classical monocyte subsets. Finally, MFI of CD31 on classical and intermediated monocyte subsets in severe/critical group were both lower than those in mild/moderate group, showing no statistical difference in MFI of CD31 on non-classical monocyte subset across groups of different disease severity. Conclusion The ratio of classical and intermediated monocyte subsets to total monocytes are correlated with the course of HFRS, and so are the surface intensity of CD31 on these monocyte subsets with the disease course and severity. The surface intensity of CD31 on non-classical monocyte subsets, however, is correlated only with the course of the disease. Together, the underlying mechanisms for the observed changes in monocyte subsets in HFRS patients should be further investigated.

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