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首页> 外文期刊>Radiation Research: Official Organ of the Radiation Research Society >A Chromosome 6, not Natural Killer Cell, Contribution to Radiation- and Bleomycin-Induced Lung Disease in Mice
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A Chromosome 6, not Natural Killer Cell, Contribution to Radiation- and Bleomycin-Induced Lung Disease in Mice

机译：染色体6，不是天然杀手细胞，对小鼠的辐射和博莱霉素诱导的肺病贡献

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摘要

Inbred strains of mice differ in susceptibility to both radiation-induced and bleomycin-induced pulmonary fibrosis and these traits have been mapped to a common locus on chromosome 6 which harbors genes of natural killer cell function. To investigate this putative locus of fibrosis susceptibility we assessed the fibrotic response of chromosome-6 consomic mice (B6.6A), and of mice deficient for natural killer cells, C57BL/6J Ly49A transgenic mice, after each of thoracic irradiation and bleomycin treatment via osmotic minipump. Thoracic irradiation resulted in less than 15% survival at 26 weeks in parental strain C57BL/6J and A/J mice, due to the development of pneumonitis with fibrosis in C57BL/6J (B6) mice, and pneumonitis in A/J mice. One hundred percent of consomic B6.6A mice survived at 26 weeks after thoracic irradiation, and developed a fibrosis level similar to that of fibrosis-resistant A/J mice, after irradiation (P = 038) or bleomycin challenge (P = 0.32). C57BL/63 Ly49A transgenic mice were confirmed through flow cytometric analysis to be deficient in NK cells, but the post-irradiation survival of these mice was not significantly different from that of wild-type littermate mice (P = 0.64). Extent of pulmonary fibrosis by histological examination did not differ between C57BL/6J Ly49A transgenic mice and wild-type littermate mice in response to either irradiation (P = 0.14) or bleomycin treatment (P = 0.62). We conclude that chromosome 6 genes, but not NK cells, contribute to the susceptibility to both radiation-induced and bleomycin-induced pulmonary fibrosis of C57BL/6J mice. (C) 2018 by Radiation Research Society
机译：小鼠的近铬菌株对辐射诱导和博来霉素诱导的肺纤维化的易感性不同，并且这些性状被映射到染色体6上的共同轨迹，其中天然杀伤细胞功能的母杀虫功能。为了调查这种纤维化敏感性的推定轨迹，我们评估了染色体-6多个小鼠（B6.6a）的纤维化反应，以及天然杀伤细胞的小鼠C57BL / 6J LY49A转基因小鼠，通过渗透微型泵。由于C57BL / 6J（B6）小鼠的纤维化，肺炎和A / J小鼠中的肺炎，胸部菌株C57BL / 6J和A / J小鼠中，胸部辐照在父母菌株C57BL / 6J和A / J小鼠中生存率小于15％。百分之百的多种多种子体B6.6a小鼠在胸部照射后26周存活，并且在照射（P = 038）或玻璃霉素攻击后（P = 0.32），产生类似于纤维化A / J小鼠的纤维化水平。通过流式细胞术分析证实C57BL / 63 Ly49a转基因小鼠在NK细胞中缺乏，但是这些小鼠的后照射后存活与野生型偶体小鼠的后照射生存率没有显着差异（p = 0.64）。通过组织学检查的肺纤维化程度在C57BL / 6JLY49A转基因小鼠和野生型凋落物小鼠之间没有差异，响应于辐照（P = 0.14）或玻璃霉素处理（P = 0.62）。我们得出结论，染色体6个基因，但不是NK细胞，有助于对辐射诱导的辐射诱导和博莱霉素诱导的C57BL / 6J小鼠肺纤维化的敏感性。 （c）2018由辐射研究协会

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