肠道炎症针对微生物群的致癌活性
Janelle C Arthur1, Ernesto Perez-Chanona, Marcus Mühlbauer
1Department of Medicine, Pharmacology and Immunology-Microbiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
概括
炎症通过改变肠道微生物促进结肠直肠癌 (CRC). 一种特定的细菌,大肠杆菌,携带一种基因毒性岛屿,驱动敏感小鼠的瘤生长,突出了预防CRC的微生物标.
科学领域:
- 微生物学 微生物学
- 在瘤学瘤学.
- 胃肠病学 胃肠病学
背景情况:
- 炎症是已知的结直肠癌 (CRC) 发展的驱动因素.
- 人们越来越认识到肠道微生物群在与炎症相关的CRC中的作用.
研究的目的:
- 研究肠道微生物群的炎症诱导变化如何影响结肠直肠癌的进展.
- 在大肠炎模型中识别导致瘤发生的特定微生物因素.
主要方法:
- 使用了易患大肠炎的互白素-10缺乏 (Il10(-/-)) 鼠标.
- 用阿佐西米 (AOM) 诱导CRC,并用大肠杆菌NC101进行单一殖民.
- 采用高通量测序来分析肠道微生物组成.
- 产生了缺乏pks的大肠杆菌菌株,以评估聚基酸合成酶基因毒性岛屿的作用.
主要成果:
- 在Il10(-/-) 小鼠中,炎症改变了肠道微生物组成.
- 用大肠杆菌 (E. coli) 的单一殖民化NC101在接受AOM治疗的Il10(-/-) 小鼠中促进了侵入性癌症.
- 从大肠杆菌中删除pks遗传毒性岛屿可以减少瘤的多重性和入侵,而不会影响炎症.
- 在人类炎症性肠病和CRC患者中发现了大肠杆菌.
结论:
- 大肠炎通过改变微生物组成和扩大遗传毒性细菌来促进CRC瘤发生.
- 大肠杆菌的pks遗传毒性岛屿有助于CRC的进展.
- 向基因毒性细菌可能提供预防或治疗CRC的策略.
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