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通过抑制IgA+B细胞和纽蛋白乙酰化促进结肠炎向结直肠癌的转变。

promotes colitis to colorectal cancer transition through IgA+ B cell suppression and vinculin acetylation.

作者信息

Zheng Jing, Zhou Chishun, Li Zizheng, Jin Xin, Zou Yihua, Bai Shasha, Zheng Huanjin, Ling Weichao, Zhao Yiru, Wang Ying, Zhang Rong, Liu Zhongqiu, Lu Linlin

机构信息

Guangdong Provincial Key Laboratory of Translational Cancer Research of Chinese Medicines, Joint International Research Laboratory of Translational Cancer Research of Chinese Medicines, International Institute for Translational Chinese Medicine, School of Pharmaceutical Sciences, State Key Laboratory of Traditional Chinese Medicine Syndrome, State Key Laboratory of Dampness Syndrome of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.

Department of Colorectal Surgery, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.

出版信息

Gut Microbes. 2025 Dec;17(1):2473511. doi: 10.1080/19490976.2025.2473511. Epub 2025 Mar 6.

DOI:10.1080/19490976.2025.2473511
PMID:40047249
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11901412/
Abstract

Lymphoid tissue-resident commensal bacteria (LRC), a subtype of gut microbiota essential for inflammation-associated carcinogenesis, predominantly attribute to colorectal cancer(CRC), whereas its role was largely unknown. Herein, we found (), the main LRC embedded in Peyer's patches, was abundantly enriched in colitis, adenoma, and stage-dependently observed in CRC tissues. Interestingly, alone can not affect intestinal homeostasis, while during colitis, significantly translocated from Peyer's patches to colon, remarkably attenuated immune response abilities of B cells, T cells, and DC cells in PPs, consequently impeded IgA+ B cells homing. Meanwhile, during colitis, the ectopia of in colon tissues, promoted vinculin acetylation by -derived metabolite acetic acid, which impeded intestinal barrier via hindering the binding of vinculin to β-catenin. Our study revealed not only suppress mucosal immune responses via reducing IgA+ B cells in Peyer's patches but also disrupt intestinal barrier via increasing vinculin acetylation, ultimately promoting inflammation-to-cancer transition in CRC.

摘要

淋巴组织驻留共生菌（LRC）是肠道微生物群的一种亚型，对炎症相关致癌作用至关重要，主要与结直肠癌（CRC）有关，但其作用在很大程度上尚不清楚。在此，我们发现，位于派尔集合淋巴结中的主要LRC在结肠炎、腺瘤中大量富集，并在CRC组织中呈阶段依赖性观察到。有趣的是，单独存在时不会影响肠道稳态，但在结肠炎期间，会从派尔集合淋巴结显著转移至结肠，显著减弱派尔集合淋巴结中B细胞、T细胞和树突状细胞（DC细胞）的免疫反应能力，从而阻碍IgA+B细胞归巢。同时，在结肠炎期间，结肠组织中的异位会通过其衍生代谢产物乙酸促进纽蛋白乙酰化，这通过阻碍纽蛋白与β-连环蛋白的结合而破坏肠道屏障。我们的研究表明，不仅通过减少派尔集合淋巴结中的IgA+B细胞来抑制黏膜免疫反应，还通过增加纽蛋白乙酰化来破坏肠道屏障，最终促进CRC中的炎症向癌症转变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/ba22920e39b5/KGMI_A_2473511_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/5a3d27979770/KGMI_A_2473511_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/6ce6c48019f2/KGMI_A_2473511_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/6e6df3312bf9/KGMI_A_2473511_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/96ec86f60597/KGMI_A_2473511_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/ecb3c9d406bc/KGMI_A_2473511_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/ac1567305bd1/KGMI_A_2473511_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/7a8e24b45070/KGMI_A_2473511_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/ba22920e39b5/KGMI_A_2473511_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/5a3d27979770/KGMI_A_2473511_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/6ce6c48019f2/KGMI_A_2473511_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/6e6df3312bf9/KGMI_A_2473511_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/96ec86f60597/KGMI_A_2473511_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/ecb3c9d406bc/KGMI_A_2473511_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/ac1567305bd1/KGMI_A_2473511_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/7a8e24b45070/KGMI_A_2473511_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25a7/11901412/ba22920e39b5/KGMI_A_2473511_F0007_OC.jpg

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