Science:肠道细菌可帮助治疗癌症
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据两项刊登在《科学》上的最新研究报告称,生活在我们肠道中的细菌群落可帮助确定某些抗癌疗法的功效,其中包括那些先前被认为直接作用于肿瘤细胞的药物。
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据两项刊登在《科学》上的最新研究报告称,生活在我们肠道中的细菌群落可帮助确定某些抗癌疗法的功效,其中包括那些先前被认为直接作用于肿瘤细胞的药物。
在这两种情况下,肠道微生物群似乎能调节由这些治疗所引发的免疫系统的反应。研究人员发现,在肠道无菌的小鼠中,这些疗法在攻击肿瘤上的效果较差。
在第一项研究中,来自美国国家癌症研究所等机构的科学家发现,抗癌免疫疗法及一种铂类化疗都对没有肠道微生物群的小鼠效果较差。在这种情况下,需要有细菌来激活某种抗肿瘤的先天免疫反应。
而在由法国古斯塔夫·鲁西癌症研究所(Institut Gustave Roussy)领导的另一项小鼠研究则表明,细胞毒性药物环磷酰胺会驱使某些细菌从肠道进入次级淋巴系统,在那里,它们会触发特殊的T“辅助”细胞及适应性免疫系统中的其它成分的产生并对肿瘤发动攻击。在没有肠道细菌的小鼠中,这一抗癌防御的激活不良。
这两项小鼠研究的数据是否反映了在接受化疗的癌症病人中所发生的情况还有待确定。如果真是这种情况,这项结果表明,可通过操纵肠道微生物群来提高某些抗癌治疗的功效。同时,它也凸显了在某些癌症治疗时使用抗菌药物会有潜在的风险。(转化医学网360zhyx.com)
原文链接:
Commensal Bacteria Control Cancer Response to Therapy by Modulating the Tumor Microenvironment
The gut microbiota influences both local and systemic inflammation. Inflammation contributes to development, progression, and treatment of cancer, but it remains unclear whether commensal bacteria affect inflammation in the sterile tumor microenvironment. Here, we show that disruption of the microbiota impairs the response of subcutaneous tumors to CpG-oligonucleotide immunotherapy and platinum chemotherapy. In antibiotics-treated or germ-free mice, tumor-infiltrating myeloid-derived cells responded poorly to therapy, resulting in lower cytokine production and tumor necrosis after CpG-oligonucleotide treatment and deficient production of reactive oxygen species and cytotoxicity after chemotherapy. Thus, optimal responses to cancer therapy require an intact commensal microbiota that mediates its effects by modulating myeloid-derived cell functions in the tumor microenvironment. These findings underscore the importance of the microbiota in the outcome of disease treatment.
The Intestinal Microbiota Modulates the Anticancer Immune Effects of Cyclophosphamide
The Intestinal Microbiota Modulates the Anticancer Immune Effects of Cyclophosphamide
Cyclophosphamide is one of several clinically important cancer drugs whose therapeutic efficacy is due in part to their ability to stimulate antitumor immune responses. Studying mouse models, we demonstrate that cyclophosphamide alters the composition of microbiota in the small intestine and induces the translocation of selected species of Gram-positive bacteria into secondary lymphoid organs. There, these bacteria stimulate the generation of a specific subset of “pathogenic” T helper 17 (pTH17) cells and memory TH1 immune responses. Tumor-bearing mice that were germ-free or that had been treated with antibiotics to kill Gram-positive bacteria showed a reduction in pTH17 responses, and their tumors were resistant to cyclophosphamide. Adoptive transfer of pTH17 cells partially restored the antitumor efficacy of cyclophosphamide. These results suggest that the gut microbiota help shape the anticancer immune response.
来源:bio360
来源:bio360
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