Division of Infectious Disease, Northwell Health, Manhasset, NY, USA.
Department of Microbiology and Immunology, University of Miami, Miller School of Medicine, Miami, FL, USA.
Sci Rep. 2019 Apr 12;9(1):5963. doi: 10.1038/s41598-019-41588-1.
The chemokine (C-C motif) chemokine ligand 18 (CCL18) is a structural homolog of CCL3 primarily produced by monocyte-derived cells with an M2 phenotype. Elevated levels of CCL18 have been observed in several diseases associated with malignancies and chronic inflammation. The role of CCL18 in Human Immunodeficiency Virus (HIV-1) infection remains unknown. We analyzed expression levels of T helper cell-mediated (TH2) chemokines CCL18, CCL17, and CCL22 by ELISA in plasma collected from HIV-1-infected and healthy donors. In HIV-1-infected individuals, plasma viral loads were monitored by NucliSense HIV-1 QT assay and T cell counts and expression of the activation marker CD38 were determined by flow cytometry. Our data showed a significant increase in plasma levels of CCL18 in HIV-1-infected individuals compared to uninfected controls (p < 0.001) and a significant correlation between CCL18 levels and viral load in untreated patients. No significant difference of CCL18 levels was detected among the HIV-1-infected patients treated with combined antiretroviral therapy (cART) and HIV-1-untreated patients.CCL18 values are negatively correlated with CD4+CD38+ cell numbers and total CD4+ T cell counts in patients with a suppressed viral load. Notably, plasma levels of the TH2 chemokines CCL17 and CCL22 are also elevated during HIV-1 infection. However, no correlation of CCL17 and CCL22 production with CD4+ T cell counts was detected. Presented data shows that the chemokines, CCL17, CCL18, and CCL22 are increased during HIV-1 infection. However, only increased levels of CCL18, a marker of M2 macrophages, correlate with low CD4+ T cell counts in patients with suppressed viral load, raising the possibility that CCL18 and/or CCL18-producing cells may interfere with their reconstitution in HIV-1-infected patients on cART.
趋化因子（C-C 基序）趋化因子配体 18（CCL18）是 CCL3 的结构同源物，主要由具有 M2 表型的单核细胞衍生细胞产生。在几种与恶性肿瘤和慢性炎症相关的疾病中，CCL18 的水平升高。CCL18 在人类免疫缺陷病毒（HIV-1）感染中的作用尚不清楚。我们通过酶联免疫吸附试验（ELISA）分析了从 HIV-1 感染和健康供体中收集的血浆中辅助性 T 细胞介导（TH2）趋化因子 CCL18、CCL17 和 CCL22 的表达水平。在 HIV-1 感染者中，通过 NucliSense HIV-1 QT 检测法监测血浆病毒载量，通过流式细胞术测定 T 细胞计数和激活标志物 CD38 的表达。我们的数据显示，与未感染对照相比，HIV-1 感染者血浆 CCL18 水平显著升高（p < 0.001），未经治疗的患者中 CCL18 水平与病毒载量之间存在显著相关性。在接受联合抗逆转录病毒治疗（cART）和未接受 HIV-1 治疗的 HIV-1 感染者中，CCL18 水平无显著差异。CCL18 值与病毒载量受抑制患者的 CD4+CD38+细胞数和总 CD4+T 细胞计数呈负相关。值得注意的是，TH2 趋化因子 CCL17 和 CCL22 的血浆水平在 HIV-1 感染期间也升高。然而，未检测到 CCL17 和 CCL22 产生与 CD4+T 细胞计数相关。本研究数据表明，趋化因子 CCL17、CCL18 和 CCL22 在 HIV-1 感染期间增加。然而，仅 CCL18（M2 巨噬细胞的标志物）的水平升高与病毒载量受抑制患者的低 CD4+T 细胞计数相关，这增加了 CCL18 和/或 CCL18 产生细胞可能干扰接受 cART 的 HIV-1 感染者 CD4+T 细胞重建的可能性。
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