Early high expression of IP-10 in F344 rats resistant to Sendai virus-induced airway injury.
Early high expression of IP-10 in F344 rats resistant to Sendai virus-induced airway injury.
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IP-10在抵抗仙台病毒诱导的气道损伤的F344大鼠中早期高表达。
DOI：
10.1152/ajplung.00274.2002
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Castleman,WilliamL
中科院分区：
文献类型：
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作者：
Cai,Xuezhong;Castleman,WilliamL
断乳F344和BN大鼠对仙台病毒诱导的气道损伤的易感性明显不同。控制其易感性差异的早期基因表达仍然知之甚少。在这项研究中，我们结合抑制性消减杂交和cDNA文库阵列杂交，以确定差异表达的基因在病毒易感BN和病毒抵抗F344大鼠在接种后的第一个3天。通过定量RT-PCR进一步验证所选克隆的差异表达。鉴定了七个病毒诱导的基因片段。其中，感染F344大鼠的干扰素-γ-诱导蛋白10（IP-10）、Mx 1和鸟苷酸结合蛋白-2（Guany-late-binding protein-2）mRNA丰度在接种后第2天分别比感染BN大鼠高201.5%、188.2%和281.7%。原位杂交结果显示，病毒诱导的IP-10主要表达于F344大鼠气道上皮细胞。仙台病毒感染可直接诱导体外培养的大鼠气管上皮细胞表达IP-10。IP-10早期高表达可能通过促进Th 1应答和增强抗病毒活性而参与F344大鼠对病毒诱导的气道疾病的抵抗。
Weanling F344 and BN rats differ markedly in their susceptibility to Sendai virus-induced airway injury. Early gene expression that controls their differences in susceptibility remains poorly understood. In this study we combined suppressive subtractive hybridization and cDNA library array hybridization to identify genes differentially expressed in virus-susceptible BN and virus-resistant F344 rats during the first 3 days after inoculation. Differential expression of selected clones was further verified by quantitative RT-PCR. Seven virus-induced gene segments were identified. Of them, interferon-γ-inducible protein 10 (IP-10), Mx1, and guany-late-binding protein-2 mRNA abundance in infected F344 rats was 201.5, 188.2, and 281.7% higher, respectively, than that of infected BN rats at 2 days after inoculation. In situ hybridization indicated that virus-induced IP-10 was expressed mainly in airway epithelial cells of F344 rats. Sendai virus infection can directly induce IP-10 expression in rat tracheal epithelial cells in vitro. IP-10 early high expression might contribute to the resistance to virus-induced airway disease in F344 rats by promoting Th1 responses and increasing antiviral activity.