Analysis of the function of CCL1 during respiratory tract infection in C-C motif ligand-1 transgenic mouse

我们利用肺内过表达CCL1基因的表面活性蛋白C启动子(SPC-CCL1TG)构建了CCL1(NCBI：rs2282691)转基因小鼠。我们在SPC-CCL1TG小鼠上建立了牛分枝杆菌卡介苗(BCG)感染模型。显微镜下观察发现，SPC-CCL1TG小鼠肺部肉芽肿数量明显增加。在DNA芯片分析中，4,569个基因在转基因小鼠的肺组织中的表达是WT小鼠的3倍或1/3或1/3。对这些基因的系统聚类分析表明，与野生型小鼠相比，在内质网应激和肉芽肿形成中起重要作用的Ern1在BCG治疗的SPC-CCL1转基因小鼠的肺中表达更高。CCL1过表达增加了BCG感染后肺肉芽肿的形成。SPC-CCL1TG小鼠与野生型小鼠相比，Ern1基因表达显著增强。

We generated the CCL1 (NCBI: rs2282691) transgenic mice using surfactant protein C promoter (SPC-CCL1 Tg), which overexpressed CCL1 gene in the lungs. We developed the Mycobacterium bovis Bacillus Calmette Guérin (BCG) infection models in SPC-CCL1 Tg mice.Microscopic observation revealed that the numbers of granulomas in the lungs were significantly increased in SPC-CCL1 Tg mice. In DNA microarray analyses, 4,569 genes had 3 times and higher or one third and lower expression in the lung of Tg mice compare to that of WT mouse. Hierarchical cluster analysis of those genes revealed that Ern1, that plays important roles in endoplasmic reticulum stress and in granuloma formation, was more upregulated in the lung of BCG-treated SPC-CCL1 Tg mice compared to that of wild type mice.CCL1 overexpression increased the formation of granulomas upon BCG infection in the lungs. SPC-CCL1 Tg mice showed significant gene expression of Ern1 in comparison with wild type mice.