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综述文章:细菌在炎症性肠病发病及持续发展中的作用

Review article: the role of bacteria in onset and perpetuation of inflammatory bowel disease.

作者信息

Seksik P, Sokol H, Lepage P, Vasquez N, Manichanh C, Mangin I, Pochart P, Doré J, Marteau P

机构信息

Département d'Hépato-Gastroentérologie, Hôpital Saint-Antoine, AP-HP, Paris, France.

出版信息

Aliment Pharmacol Ther. 2006 Oct;24 Suppl 3:11-8. doi: 10.1111/j.1365-2036.2006.03053.x.

Abstract

We review the evidence that strongly suggests a role of the intestinal microbiota in the onset and perpetuation of inflammatory bowel disease (IBD). Experimental studies consisted of suppressing micro-organisms from the microbiota (using germ-free or gnotoxenic animals or antibiotics), introducing new micro-organisms or microbial components (e.g. probiotics, CpG-DNA) or selectively increasing some endogenous bacteria (e.g. using prebiotics). Intervention studies were performed in patients or animal models of spontaneous or chemically-induced colitis. Information was also obtained from observational studies that described the composition of the faecal and mucosal microbiota at various stages of the disease process and in controls. Many have used culture-independent techniques that identify bacteria based on the nucleic acid sequence of ribosomal RNA molecules. Microbiota in patients with IBD seem to be characterized by high concentrations of bacteria in contact with the mucosa, instability, the presence of high numbers of unusual bacteria and sometimes a reduction in the biodiversity. Studies searching for a generalized or localized dysbiosis in IBD are discussed, as well as those trying to identify bacterial molecules and receptors, which may be implicated in triggering the inflammatory process.

摘要

我们回顾了有力证据,这些证据强烈表明肠道微生物群在炎症性肠病(IBD)的发病及持续发展中发挥作用。实验研究包括从微生物群中抑制微生物(使用无菌或悉生动物或抗生素)、引入新的微生物或微生物成分(如益生菌、CpG-DNA)或选择性增加一些内源性细菌(如使用益生元)。干预研究在自发性或化学诱导性结肠炎的患者或动物模型中进行。还从观察性研究中获取了信息,这些研究描述了疾病过程不同阶段以及对照中粪便和黏膜微生物群的组成。许多研究使用了不依赖培养的技术,这些技术基于核糖体RNA分子的核酸序列来鉴定细菌。IBD患者的微生物群似乎具有与黏膜接触的细菌浓度高、不稳定、存在大量异常细菌以及有时生物多样性降低的特征。文中讨论了寻找IBD中普遍或局部生态失调的研究,以及试图鉴定可能与引发炎症过程有关的细菌分子和受体的研究。

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