Elevated Plasma Fractalkine Level Is Associated with the Severity of Hemorrhagic Fever with Renal Syndrome in Humans.
Elevated Plasma Fractalkine Level Is Associated with the Severity of Hemorrhagic Fever with Renal Syndrome in Humans.
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DOI：
10.1089/vim.2020.0244
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发表时间：
2021-08
期刊：
影响因子：
2.2
通讯作者：
Chunmei Zhang;K. Tang;Yusi Zhang;Ying Ma;H. Du;Xuyang Zheng;Kun Yang;Lihua Chen;R. Zhuang;Boquan Jin;Yun Zhang
中科院分区：
文献类型：
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作者：
Chunmei Zhang;K. Tang;Yusi Zhang;Ying Ma;H. Du;Xuyang Zheng;Kun Yang;Lihua Chen;R. Zhuang;Boquan Jin;Yun Zhang
汉滩病毒感染可引起人类严重致死性肾综合征出血热（HFRS）。趋化因子fractalkine（CX 3CL 1）作为一种促炎细胞因子，在几种感染性疾病中升高。然而，对CX 3CL 1在HFRS发病机制中的作用知之甚少。本研究通过检测肾综合征出血热患者血浆CX 3CL 1水平及其受体CX 3CR 1的表达，探讨CX 3CL 1在肾综合征出血热发病机制中的可能作用。HFRS患者急性期和危重/重症组血浆CX 3CL 1较正常对照组明显升高（分别为p < 0.001和p < 0.01）。高血浆CX 3 CL 1与血小板计数呈负相关（r =-0.5844，p < 0.0001），与血尿素氮（r = 0.3668，p = 0.0039）、肌酐（r = 0.42，p = 0.0008）和白色细胞（r = 0.2646，p = 0.0411）呈正相关。与正常对照组相比，HFRS患者急性期（两种细胞均P < 0.01）和危重/重症组（分别P < 0.05和P < 0.01）的非经典和中间型单核细胞上的CX 3CR 1表达也增加。总之，HFRS患者血浆中CX 3CL 1的升高以及CX 3CR 1在非经典和中间单核细胞亚群上的表达可能为CX 3CL 1/CX 3CR 1在HFRS发病机制中的潜在作用提供新的见解。
Hantaan virus infection may cause severe lethal hemorrhagic fever with renal syndrome (HFRS) in humans. The chemokine fractalkine (CX3CL1) acts as a proinflammatory cytokine, and it is elevated in several infectious diseases. However, little is known about the contributions of CX3CL1 to HFRS pathogenesis. Present study detected plasma CX3CL1 levels and expression of the receptor CX3CR1 in HFRS patients and discussed the possible effects of CX3CL1 on pathogenesis of HFRS. Plasma CX3CL1 in acute phase and Critical/Severe groups of HFRS patients were significantly increased compared to that in normal controls (p < 0.001 and p < 0.01, respectively). High plasma CX3CL1 was negatively correlated with platelet count (r = -0.5844, p < 0.0001) and positively correlated with blood urea nitrogen (r = 0.3668, p = 0.0039), creatinine (r = 0.42, p = 0.0008), and white blood cells (r = 0.2646, p = 0.0411). Expression of CX3CR1 on nonclassical and intermediate monocytes was also increased in the acute phase (p < 0.01 for both the cells) and Critical/Severe groups (p < 0.05 and p < 0.01, respectively) of HFRS patients compared to that in normal controls. Taken together, elevation of plasma CX3CL1 in HFRS patients and expression of CX3CR1 on nonclassical and intermediate monocyte subsets might provide new insights into the potential role of CX3CL1/CX3CR1 in pathogenesis of HFRS.