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肠道微生物群通过丁酸介导的改变肠道屏障功能来调节急性髓系白血病。

Gut microbiota regulates acute myeloid leukaemia via alteration of intestinal barrier function mediated by butyrate.

机构信息

Department of Hematology, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, P. R. China.

Department of Endocrinology and Metabolism, Shandong Provincial Hospital affiliated with Shandong University, Jinan, Shandong, 250012, P. R. China.

出版信息

Nat Commun. 2022 May 9;13(1):2522. doi: 10.1038/s41467-022-30240-8.

DOI:10.1038/s41467-022-30240-8
PMID:35534496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9085760/
Abstract

The gut microbiota has been linked to many cancers, yet its role in acute myeloid leukaemia (AML) progression remains unclear. Here, we show decreased diversity in the gut microbiota of AML patients or murine models. Gut microbiota dysbiosis induced by antibiotic treatment accelerates murine AML progression while faecal microbiota transplantation reverses this process. Butyrate produced by the gut microbiota (especially Faecalibacterium) significantly decreases in faeces of AML patients, while gavage with butyrate or Faecalibacterium postpones murine AML progression. Furthermore, we find the intestinal barrier is damaged in mice with AML, which accelerates lipopolysaccharide (LPS) leakage into the blood. The increased LPS exacerbates leukaemia progression in vitro and in vivo. Butyrate can repair intestinal barrier damage and inhibit LPS absorption in AML mice. Collectively, we demonstrate that the gut microbiota promotes AML progression in a metabolite-dependent manner and that targeting the gut microbiota might provide a therapeutic option for AML.

摘要

肠道微生物群与许多癌症有关，但它在急性髓系白血病 (AML) 进展中的作用仍不清楚。在这里，我们表明 AML 患者或小鼠模型的肠道微生物群多样性降低。抗生素治疗引起的肠道微生物群失调会加速小鼠 AML 的进展，而粪便微生物群移植则逆转了这一过程。肠道微生物群（尤其是粪杆菌）产生的丁酸盐在 AML 患者的粪便中显著减少，而丁酸盐或粪杆菌灌胃可延缓小鼠 AML 的进展。此外，我们发现 AML 小鼠的肠道屏障受损，这会加速脂多糖 (LPS) 漏入血液。增加的 LPS 在体外和体内加剧了白血病的进展。丁酸盐可修复 AML 小鼠的肠道屏障损伤并抑制 LPS 吸收。总之，我们证明了肠道微生物群以代谢物依赖的方式促进 AML 的进展，而靶向肠道微生物群可能为 AML 提供一种治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/3924d7811044/41467_2022_30240_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/8af3f4d527a6/41467_2022_30240_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/8c0477cfa721/41467_2022_30240_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/d8bdcbbb7c18/41467_2022_30240_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/97ae9f6e9c5f/41467_2022_30240_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/259b95e0d2db/41467_2022_30240_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/f6ce24ee1f20/41467_2022_30240_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/47f2e47c1a48/41467_2022_30240_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/3924d7811044/41467_2022_30240_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/8af3f4d527a6/41467_2022_30240_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/8c0477cfa721/41467_2022_30240_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/d8bdcbbb7c18/41467_2022_30240_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/97ae9f6e9c5f/41467_2022_30240_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/259b95e0d2db/41467_2022_30240_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/f6ce24ee1f20/41467_2022_30240_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/47f2e47c1a48/41467_2022_30240_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7967/9085760/3924d7811044/41467_2022_30240_Fig8_HTML.jpg

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