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乳糜泻患者肠道微生物群的改变及其益生菌调节作用

Gut Microbiota Alteration and Its Modulation with Probiotics in Celiac Disease.

作者信息

Saviano Angela, Petruzziello Carmine, Brigida Mattia, Morabito Loprete Maria Rita, Savioli Gabriele, Migneco Alessio, Ojetti Veronica

机构信息

Department of Emergency Medicine, Fondazione Policlinico Universitario A. Gemelli, IRCCS, 00168 Rome, Italy.

Department of Emergency Medicine, Ospedale San Carlo di Nancy, GVM Care and Research, 00165 Rome, Italy.

出版信息

Biomedicines. 2023 Sep 26;11(10):2638. doi: 10.3390/biomedicines11102638.

Abstract

Celiac disease (CD) is a chronic inflammation of the small intestine triggered by gluten ingestion in genetically predisposed people. Recent literature studies highlight the possible role of the gut microbiota in the pathogenesis of this disease. The gut microbiota is a complex community of microorganisms that can interact with the innate and adaptative immune systems. A condition of dysbiosis, which refers to an alteration in the composition and function of the human gut microbiota, can lead to a dysregulated immune response. This condition may contribute to triggering gluten intolerance, favoring the development and/or progression of CD in genetically susceptible patients. Interestingly, studies on children and adults with CD showed a different microbiome profile in fecal samples, with a different degree of "activity" for the disease. From this point of view, our review aimed to collect and discuss modern evidence about the alteration of the gut microbiota and its modulation with probiotics, with possible future indications in the management of patients affected by CD.

摘要

乳糜泻(CD)是一种在具有遗传易感性的人群中,由摄入麸质引发的小肠慢性炎症。近期的文献研究强调了肠道微生物群在该疾病发病机制中的可能作用。肠道微生物群是一个复杂的微生物群落,能够与固有免疫系统和适应性免疫系统相互作用。生态失调是指人类肠道微生物群的组成和功能发生改变的一种状况,它可导致免疫反应失调。这种状况可能有助于引发麸质不耐受,促进遗传易感患者中CD的发生和/或进展。有趣的是,对患有CD的儿童和成人的研究表明,粪便样本中的微生物组谱不同,疾病的“活动”程度也不同。从这一角度来看,我们的综述旨在收集和讨论关于肠道微生物群改变及其用益生菌进行调节的现代证据,以及未来在CD患者管理方面可能的应用方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c61d/10603901/8469c4899b86/biomedicines-11-02638-g001.jpg

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