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富含硒的长双歧杆菌DD98改善肠道微生物群，通过抑制STING通路减轻化疗诱导的肠道粘膜炎。

Improved gut microbiota by selenium-enriched Bifidobacterium longum DD98 alleviates chemotherapy-induced intestinal mucositis via inhibiting the STING pathway.

作者信息

Qiu Yu-Shuang, Ye Chen, Li Qiao, Jiang Ling-Chen, Zhou Can-Can, Fu Hui, Li Dong-Jie, Chen Daijie, Shen Fu-Ming

机构信息

Department of Pharmacy, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.

Department of Colorectal Disease Specialty, Clinical Research Center for Digestive Diseases, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai, China.

出版信息

NPJ Sci Food. 2025 Jun 21;9(1):107. doi: 10.1038/s41538-025-00473-0.

DOI:10.1038/s41538-025-00473-0
PMID:40544178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12182572/
Abstract

Intestinal mucositis, a common chemotherapy side effect, lacks effective treatments. This study evaluated the protective effect of selenium-enriched Bifidobacterium longum DD98 (SeDD98) on irinotecan-induced intestinal mucositis. Irinotecan caused intestinal mucositis, characterized by weight loss, severe diarrhea, damaged intestinal structure, reduced tight junction proteins, and gut dysbiosis. These effects could be inhibited by SeDD98. Additionally, fecal microbiota from SeDD98-treated mice protected against intestinal mucositis. Mechanistically, irinotecan activated the stimulator of interferon genes (STING) / nuclear factor kappa-B (NF-κB) pathway, whereas SeDD98 and fecal microbiota from SeDD98-treated mice suppressed this activation. Furthermore, depletion of gut microbiota by a broad-spectrum antibiotic cocktail (ABX) blunted the protective effect of SeDD98 and its inhibition of the STING/NF-κB pathway. These findings suggest that SeDD98 could protect against intestinal mucositis via inhibiting the STING/NF-κB pathway, likely through improving gut microbiota. Overall, SeDD98 may be a potential therapeutic agent for preventing chemotherapy-induced intestinal mucositis via gut microbiome improvement.

摘要

肠道黏膜炎是一种常见的化疗副作用，目前缺乏有效的治疗方法。本研究评估了富硒长双歧杆菌DD98（SeDD98）对伊立替康诱导的肠道黏膜炎的保护作用。伊立替康可导致肠道黏膜炎，表现为体重减轻、严重腹泻、肠道结构受损、紧密连接蛋白减少以及肠道菌群失调。这些影响可被SeDD98抑制。此外，来自SeDD98处理小鼠的粪便微生物群可预防肠道黏膜炎。从机制上讲，伊立替康激活了干扰素基因刺激因子（STING）/核因子κB（NF-κB）通路，而SeDD98以及来自SeDD98处理小鼠的粪便微生物群可抑制这种激活。此外，广谱抗生素混合物（ABX）使肠道微生物群减少，削弱了SeDD98的保护作用及其对STING/NF-κB通路的抑制作用。这些发现表明，SeDD98可能通过抑制STING/NF-κB通路来预防肠道黏膜炎，可能是通过改善肠道微生物群实现的。总体而言，SeDD98可能是一种潜在的治疗药物，可通过改善肠道微生物群来预防化疗诱导的肠道黏膜炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b98a/12182572/904fe321f2e9/41538_2025_473_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b98a/12182572/904fe321f2e9/41538_2025_473_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b98a/12182572/97113cdb82e9/41538_2025_473_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b98a/12182572/6a7cbd4014a5/41538_2025_473_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b98a/12182572/904fe321f2e9/41538_2025_473_Fig7_HTML.jpg

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本文引用的文献

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Food Funct. 2023 Jun 6;14(11):5355-5374. doi: 10.1039/d2fo03408e.
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Viable Bifidobacterium tablets for the prevention of chemotherapy-/radiation-induced mucositis in patients undergoing haematopoietic stem cell transplantation.用于预防造血干细胞移植患者化疗/放疗引起的粘膜炎的活性双歧杆菌片
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CDK4/6 inhibitor modulating active and quiescent intestinal stem cells for prevention of chemotherapy-induced diarrhea.
CDK4/6 抑制剂调节活跃和静止的肠道干细胞以预防化疗引起的腹泻。
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Chemotherapeutic Drugs Induce Different Gut Microbiota Disorder Pattern and NOD/RIP2/NF-κB Signaling Pathway Activation That Lead to Different Degrees of Intestinal Injury.化疗药物诱导不同的肠道微生物群落紊乱模式和 NOD/RIP2/NF-κB 信号通路激活，导致不同程度的肠道损伤。
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