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钙依赖性固有免疫过程在炎症性肠病中的作用。

Ca-Dependent Processes of Innate Immunity in IBD.

机构信息

Department of Translational Medical Sciences, University of Naples Federico II, 80131 Naples, Italy.

Center for Basic and Clinical Immunology Research (CISI), University of Naples Federico II, 80131 Naples, Italy.

出版信息

Cells. 2024 Jun 21;13(13):1079. doi: 10.3390/cells13131079.

DOI:10.3390/cells13131079
PMID:38994933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11240513/
Abstract

IBD is an uncontrolled inflammatory condition of the gastrointestinal tract, which mainly manifests in two forms: ulcerative colitis (UC) and Crohn's disease (CD). The pathogenesis of IBD appears to be associated with an abnormal response of innate and adaptive immune cells. Innate immunity cells, such as macrophages, mast cells, and granulocytes, can produce proinflammatory (e.g., TNF-α) and oxidative stress (ROS) mediators promoting intestinal damage, and their abnormal responses can induce an imbalance in adaptive immunity, leading to the production of inflammatory cytokines that increase innate immune damage, abate intestinal barrier functions, and aggravate inflammation. Considering that Ca signalling plays a key role in a plethora of cellular functions, this review has the purpose of deepening the potential Ca involvement in IBD pathogenesis.

摘要

IBD 是一种胃肠道的失控性炎症性疾病,主要有两种表现形式:溃疡性结肠炎(UC)和克罗恩病(CD)。IBD 的发病机制似乎与先天和适应性免疫细胞的异常反应有关。先天免疫细胞,如巨噬细胞、肥大细胞和粒细胞,可产生促炎(如 TNF-α)和氧化应激(ROS)介质,促进肠道损伤,其异常反应可诱导适应性免疫失衡,导致炎症细胞因子的产生增加,先天免疫损伤加重,肠道屏障功能减弱,炎症加重。鉴于钙信号在众多细胞功能中发挥着关键作用,本综述旨在深入探讨钙在 IBD 发病机制中的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f0f/11240513/c7ad306e830d/cells-13-01079-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f0f/11240513/c7ad306e830d/cells-13-01079-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f0f/11240513/c7ad306e830d/cells-13-01079-g001.jpg

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本文引用的文献

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Novel approaches in IBD therapy: targeting the gut microbiota-bile acid axis.IBD 治疗的新方法:靶向肠道微生物群-胆汁酸轴。
Gut Microbes. 2024 Jan-Dec;16(1):2356284. doi: 10.1080/19490976.2024.2356284. Epub 2024 May 20.
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Neutrophils: from IBD to the gut microbiota.中性粒细胞:从炎症性肠病到肠道微生物群
Nat Rev Gastroenterol Hepatol. 2024 Mar;21(3):184-197. doi: 10.1038/s41575-023-00871-3. Epub 2023 Dec 18.
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Microbiome and metabolome features in inflammatory bowel disease via multi-omics integration analyses across cohorts.
通过跨队列的多组学整合分析探讨炎症性肠病的微生物组和代谢组特征。
Nat Commun. 2023 Nov 6;14(1):7135. doi: 10.1038/s41467-023-42788-0.
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Modulating mitochondrial calcium channels (TRPM2/MCU/NCX) as a therapeutic strategy for neurodegenerative disorders.调节线粒体钙通道(TRPM2/MCU/NCX)作为神经退行性疾病的治疗策略。
Front Neurosci. 2023 Oct 20;17:1202167. doi: 10.3389/fnins.2023.1202167. eCollection 2023.
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Intestinal Immune Imbalance is an Alarm in the Development of IBD.肠道免疫失衡是 IBD 发展的警报。
Mediators Inflamm. 2023 Jul 31;2023:1073984. doi: 10.1155/2023/1073984. eCollection 2023.
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Exploring the Pipeline of Novel Therapies for Inflammatory Bowel Disease; State of the Art Review.探索炎症性肠病新型疗法的研发进程;最新技术综述
Biomedicines. 2023 Mar 1;11(3):747. doi: 10.3390/biomedicines11030747.
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The role of Th17 cells in inflammatory bowel disease and the research progress.辅助性 T 细胞 17 在炎症性肠病中的作用及研究进展。
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Pathophysiology of Inflammatory Bowel Disease: Innate Immune System.炎症性肠病的病理生理学:固有免疫系统。
Int J Mol Sci. 2023 Jan 12;24(2):1526. doi: 10.3390/ijms24021526.
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Int Immunopharmacol. 2023 Feb;115:109655. doi: 10.1016/j.intimp.2022.109655. Epub 2022 Dec 31.
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