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宿主免疫与感染之间的相互作用。

The interplay between host immunity and infection.

作者信息

Li Danyang, Saavedra Pedro H V

机构信息

Department of Biology, Northeastern University, Boston, Massachusetts, USA.

出版信息

mBio. 2025 Aug 13;16(8):e0356224. doi: 10.1128/mbio.03562-24. Epub 2025 Jul 1.

DOI:10.1128/mbio.03562-24
PMID:40590563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12345233/
Abstract

infection (CDI) is a major public health concern and the leading cause of healthcare-associated infectious enteric inflammation worldwide. Disruption of the gut microbiome predisposes to colonization, proliferation, and production of cytotoxic toxins that damage the intestinal epithelial layer. CDI treatment is challenging in part due to the emergence of antibiotic-resistant strains and the lack of efficient vaccines, predisposing individuals to recurrent CDI episodes. Consequently, there is an urgent need for the development of novel therapeutic approaches. Both innate and adaptive immune responses contribute to protection against CDI, but the cellular and molecular mechanisms underlying this process are not completely understood. In this mini review, I discuss the history and recent findings with a focus on mechanisms that drive host immunity to , with a conclusion on where the field stands and outstanding questions that remain elusive.

摘要

艰难梭菌感染(CDI)是一个重大的公共卫生问题,是全球医疗保健相关感染性肠道炎症的主要原因。肠道微生物群的破坏易引发艰难梭菌的定植、增殖以及细胞毒素的产生,这些毒素会损害肠道上皮层。CDI治疗具有挑战性,部分原因是抗生素耐药菌株的出现以及缺乏有效的疫苗,这使得个体易反复发生CDI发作。因此,迫切需要开发新的治疗方法。先天性和适应性免疫反应均有助于抵御CDI,但这一过程背后的细胞和分子机制尚未完全明确。在本综述中,我将讨论艰难梭菌感染的历史和最新研究发现,重点关注驱动宿主对艰难梭菌免疫的机制,并对该领域的现状和仍未解决的突出问题进行总结。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c918/12345233/8f93c0270a51/mbio.03562-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c918/12345233/8f93c0270a51/mbio.03562-24.f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c918/12345233/8f93c0270a51/mbio.03562-24.f001.jpg

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本文引用的文献

1
IL-33 protects from recurrent C. difficile infection by restoration of humoral immunity.白细胞介素-33通过恢复体液免疫来预防艰难梭菌反复感染。
J Clin Invest. 2025 Mar 6;135(9). doi: 10.1172/JCI184659. eCollection 2025 May 1.
2
Fiber- and acetate-mediated modulation of MHC-II expression on intestinal epithelium protects from Clostridioides difficile infection.纤维和乙酸盐介导的肠道上皮细胞MHC-II表达调节可预防艰难梭菌感染。
Cell Host Microbe. 2025 Feb 12;33(2):235-251.e7. doi: 10.1016/j.chom.2024.12.017. Epub 2025 Jan 17.
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Protection against Clostridioides difficile disease by a naturally avirulent strain.
天然无毒菌株对艰难梭菌病的保护作用。
Cell Host Microbe. 2025 Jan 8;33(1):59-70.e4. doi: 10.1016/j.chom.2024.11.003. Epub 2024 Nov 27.
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Succinate-producing microbiota drives tuft cell hyperplasia to protect against Clostridioides difficile.琥珀酸产生菌驱动肠绒毛细胞增生以预防艰难梭菌感染。
J Exp Med. 2025 Jan 6;222(1). doi: 10.1084/jem.20232055. Epub 2024 Nov 26.
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NKp46 ILC3s promote early neutrophil defense against infection through GM-CSF secretion.NKp46+ ILC3s 通过分泌 GM-CSF 促进早期中性粒细胞抵御感染。
Proc Natl Acad Sci U S A. 2024 Nov 5;121(45):e2416182121. doi: 10.1073/pnas.2416182121. Epub 2024 Oct 30.
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Purified CDT toxins and a clean deletion within the CDT locus provide novel insights into the contribution of binary toxin in cellular inflammation and Clostridioides difficile infection.纯化的 CDT 毒素和 CDT 基因座内的清洁缺失为二元毒素在细胞炎症和艰难梭菌感染中的作用提供了新的见解。
PLoS Pathog. 2024 Sep 19;20(9):e1012568. doi: 10.1371/journal.ppat.1012568. eCollection 2024 Sep.
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Antibiotics damage the colonic mucus barrier in a microbiota-independent manner.抗生素以一种不依赖于微生物群的方式破坏结肠粘液屏障。
Sci Adv. 2024 Sep 13;10(37):eadp4119. doi: 10.1126/sciadv.adp4119. Epub 2024 Sep 11.
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Nat Rev Immunol. 2024 Nov;24(11):798-809. doi: 10.1038/s41577-024-01057-x. Epub 2024 Jul 15.