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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Microbial regulation of intestinal radiosensitivity
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Microbial regulation of intestinal radiosensitivity

机译：肠道放射敏感性的微生物调节

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We describe a method for treating germ-free (GF) mice with gamma-irradiation and transplanting them with normal or genetically manipulated bone marrow while maintaining their GF status. This approach revealed that GF mice are markedly resistant to lethal radiation enteritis. Furthermore, administering lethal doses of total body irradiation to GF mice produces markedly fewer apoptotic endothelial cells and lymphocytes in the mesenchymal cores of their small intestinal villi, compared with conventionally raised animals that have acquired a microbiota from birth. Analysis of GF and conventionally raised Rag1(-/-) mice disclosed that mature lymphocytes are not required for the development of lethal radiation enteritis or the microbiota-associated enhancement of endothelial radiosensitivity. Studies of gnotobiotic knockout mice that lack fasting-induced adipose factor (Fiaf), a fibrinogen/angio-poietin-like protein normally secreted from the small intestinal villus epithelium and suppressed by the microbiota, showed that Fiaf deficiency results in loss of resistance of villus endothelial and lymphocyte populations to radiation-induced apoptosis. Together, these findings provide insights about the cellular and molecular targets involved in microbial. regulation of intestinal radiosensitivity.
机译：我们描述了一种用γ射线治疗无菌（GF）小鼠并在保持其GF状态的同时将它们与正常或基因改造的骨髓一起移植的方法。这种方法表明，GF小鼠对致命的放射性肠炎具有明显的抵抗力。此外，与常规饲养的从出生时获得微生物菌群的动物相比，对GF小鼠给予致死剂量的全身照射会在其小肠绒毛的间充质核心中产生明显较少的凋亡内皮细胞和淋巴细胞。 GF和常规饲养的Rag1（-/-）小鼠的分析显示，致命的放射性肠炎或与微生物群相关的内皮细胞放射敏感性的增强不需要成熟的淋巴细胞。缺乏空腹诱导的脂肪因子（Fiaf）（通常从小肠绒毛上皮分泌并被微生物群抑制的一种纤维蛋白原/血管生成素样蛋白）的致病基因敲除小鼠的研究表明，缺乏Fiaf会导致绒毛抵抗力降低内皮细胞和淋巴细胞群能辐射诱导凋亡。这些发现共同提供了有关微生物所涉及的细胞和分子靶标的见解。调节肠道放射敏感性。

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