Tumor necrosis factor alpha and macrophages in the brain of herpes simplex virus type 1-infected BALB/c mice.
Tumor necrosis factor alpha and macrophages in the brain of herpes simplex virus type 1-infected BALB/c mice.
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单纯疱疹病毒 1 型感染的 BALB/c 小鼠大脑中的肿瘤坏死因子 α 和巨噬细胞。
DOI：
10.1080/13550280601039030
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发表时间：
2006
影响因子：
3.2
通讯作者：
Atherton,SallyS
中科院分区：
文献类型：
--
作者：
Fields,Mark;Zheng,Mei;Zhang,Ming;Atherton,SallyS
在单眼前房（AC）接种单纯疱疹病毒1型（HSV-1）后，在视交叉上核（SCN）中检测到病毒和TNF-α（TNF-α）。本研究的目的是研究TNF-α和巨噬细胞在HSV-1感染的BALB/c小鼠脑中的作用。用沙利度胺处理小鼠以抑制TNF-α或注射氯膦酸盐脂质体以消耗巨噬细胞，并在一只眼睛（同侧）的AC中注射HSV-1（科斯）。用荧光免疫组化法检测HSV-1、巨噬细胞和TNF-α的定位，空斑法检测病毒滴度。通过逆转录酶-聚合酶链反应（RT-PCR）测定TNF-α的抑制作用，并通过流式细胞术评估巨噬细胞的耗竭。在沙利度胺处理的小鼠中，SCN中的TNF-α RNA水平降低。两个SCN在接种后第5天（p.i.）注射侧对侧SCN中病毒滴度增加。与对照组相比，氯膦酸盐处理小鼠的脾巨噬细胞数量显著减少。在巨噬细胞耗尽的小鼠中，两个SCN在感染后第6天被感染。并且这些小鼠的SCN中的病毒滴度在感染后第6天和第7天增加。与对照组比较。在感染后第7天，巨噬细胞耗竭小鼠对侧（未接种）眼中的病毒滴度增加。在巨噬细胞耗竭小鼠的SCN中观察到较少的F4/80+细胞。这些研究的结果表明，TNF-α在限制正常胸腺BALB/c小鼠SCN中的病毒复制中发挥作用，并且TNF-α的一个来源是巨噬细胞。
After uniocular anterior chamber (AC) inoculation of herpes simplex virus type 1 (HSV-1), virus and TNF alpha (TNF-α) are detected in the suprachiasmatic nuclei (SCN). The goal of this study was to investigate the role of TNF-α and macrophages in the brain of HSV-1–infected BALB/c mice. Mice were treated with thalidomide for TNF-α inhibition or injected with clodronate liposomes to deplete macrophages, and the AC of one eye (ipsilateral) was injected with HSV-1 (KOS). The location of HSV-1, macrophages, and TNF-α was determined by fluorescence immunohistochemistry and the titer of virus was determined by plaque assay. Inhibition of TNF-α was determined by reverse transcriptase–polymerase chain reaction (RT-PCR) and depletion of macrophages was assessed by flow cytometry. In thalidomide-treated mice, TNF-α RNA levels were reduced in the SCN. Both SCN were infected by day 5 post inoculation (p.i.) and the titer of virus in the SCN contralateral to the side of injection was increased. The number of splenic macrophages was significantly reduced in clodronate-treated mice compared with controls. In macrophage-depleted mice, both SCN were infected at day 6 p.i. and the titer of virus in the SCN of these mice was increased at days 6 and 7 p.i. compared with controls. The titer of virus in the contralateral (uninoculated) eye of macrophage-depleted mice was increased at day 7 p.i. Fewer F4/80+cells were observed in the SCN of macrophage-depleted mice. The results of these studies suggest that TNF-α plays a role in limiting virus replication in the SCN of euthymic BALB/c mice and that one source of TNF-α is macrophages.