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

我们利用表面活性剂蛋白C启动子（SPC-CCL1 Tg）在肺中过表达CCL1基因，构建了CCL1 （NCBI: rs2282691）转基因小鼠。我们建立了SPC-CCL1 Tg小鼠卡介苗（Mycobacterium bovis Bacillus Calmette gusamrin， BCG）感染模型。显微镜观察发现，SPC-CCL1 Tg小鼠肺内肉芽肿数量明显增加。在DNA微阵列分析中，4569个基因在Tg小鼠肺中的表达量比WT小鼠高3倍或低1 / 3。这些基因的层次聚类分析显示，在内质网应激和肉芽肿形成中起重要作用的Ern1在bcg处理的SPC-CCL1 Tg小鼠的肺中比野生型小鼠表达上调。CCL1过表达增加了卡介苗感染后肺部肉芽肿的形成。SPC-CCL1 Tg小鼠与野生型小鼠相比，Ern1基因表达显著。

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.