Elevated cerebrospinal fluid levels of monocyte chemotactic protein-1 correlate with HIV-1 encephalitis and local viral replication
Elevated cerebrospinal fluid levels of monocyte chemotactic protein-1 correlate with HIV-1 encephalitis and local viral replication
复制标题
DOI：
10.1097/00002030-199811000-00014
复制
发表时间：
1998-07-30
期刊：
影响因子：
3.8
通讯作者：
Poli, G
中科院分区：
文献类型：
--
作者：
Cinque, P;Vago, L;Poli, G
目的：探讨CC趋化因子单核细胞趋化蛋白(MCP)-1在HIV中枢神经系统感染发病机制中的作用。设计和方法：检测37例有神经系统症状的HLV感染患者脑脊液中MCP-1的水平，并与尸检中HIV-1脑炎的存在和严重程度以及脑脊液中的HIV RNA水平进行比较。结果：HIV脑炎患者脑脊液MCP-1水平(中位数为4.99 ng/ml)明显高于非HIV脑炎组(中位数为1.72 ng/ml)。CMV脑炎、HIV和CMV脑炎患者的脑脊液MCP-1浓度也升高(中位数分别为3.14和4.23 ng/ml)。HIV脑炎与脑脊液中单核细胞趋化蛋白-1水平升高密切相关(P=0.002)，与脑脊液中HIV1RNA水平升高相关(P=0.007)，与血浆病毒血症无关。在体外，单核细胞来源的巨噬细胞感染HIV-1上调了MCP-1的分泌。结论：综上所述，体内和体外的研究结果支持这样一种模型，即HIV脑炎是通过小胶质细胞中的病毒复制而持续的，这一过程是通过HIV诱导的MCP-1募集单个核细胞而放大的。(C)1998年利平科特-乌鸦出版社。
Objective: To investigate whether the CC-chemokine monocyte chemotactic protein (MCP)-1 could play a role in the pathogenesis of HIV infection of the central nervous system. This hypothesis was suggested by previous observations, including our finding of elevated cerebrospinal fluid (CSF) levels of this chemokine in patients with cytomegalovirus (CMV) encephalitis.Design and methods: CSF levels of MCP-1 were determined in 37 HlV-infected patients with neurological symptoms, and were compared with both the presence and severity of HIV-1 encephalitis at post-mortem examination and CSF HIV RNA levels. MCP-1 production by monocyte-derived macrophages was tested after in vitro infection of these cells by HIV.Results: CSF MCP-1 levels were significantly higher in patients with (median, 4.99 ng/ml) than in those without (median, 1.72 ng/ml) HIV encephalitis. Elevated CSF MCP-1 concentrations were also found in patients with CMV encephalitis and with concomitant HIV and CMV encephalitis (median, 3.14 and 4.23 ng/ml, respectively). HIV encephalitis was strongly associated with high CSF MCP-1 levels (P = 0.002), which were also correlated to high HIV-1 RNA levels in the CSF (P = 0.007), but not to plasma viraemia. In vitro, productive HIV-1 infection of monocyte-derived macrophages upregulated the secretion of MCP-1.Conclusions: Taken together, these in vivo and in vitro findings support a model whereby HIV encephalitis is sustained by virus replication in microglial cells, a process amplified by recruitment of mononuclear cells via HIV-induced MCP-1. (C) 1998 Lippincott-Raven Publishers.