Department of Medicine, Mater Dei Hospitalgrid.414826.d, Msida, Malta.
Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany.
Microbiol Spectr. 2022 Jun 29;10(3):e0061622. doi: 10.1128/spectrum.00616-22. Epub 2022 May 9.
Inflammatory bowel disease (IBD) is a chronic, relapsing, inflammatory disorder which comprises two main conditions: Crohn's disease (CD) and ulcerative colitis (UC). Although the etiology of IBD has not been fully elucidated, the gut microbiota is hypothesized to play a vital role in its development. The aim of this cross-sectional study was to characterize the fecal microbiota in CD or UC patients in a state of remission to reveal potential factors sustaining residual levels of inflammation and triggering disease relapses. Ninety-eight IBD patients in a state of clinical remission (66 UC, 32 CD) and 97 controls were recruited, and stool samples, as well as detailed patient data, were collected. After DNA extraction, the variable regions V1 and V2 of the 16S rRNA gene were amplified and sequenced. Patients with IBD had a decrease in alpha diversity compared to that of healthy controls, and the beta diversity indices showed dissimilarity between the cohorts. Healthy controls were associated with the beneficial organisms unclassified species (.), ., and ., while flavonoid-degrading bacteria were associated with IBD. Network analysis identified highly central and influential disease markers and a strongly correlated network module of which was associated with IBD and could act as drivers for residual inflammatory processes sustaining and triggering IBD, even in a state of low disease activity. The microbiota in IBD patients is significantly different from that of healthy controls, even in a state of remission, which implicates the microbiota as an important driver of chronicity in IBD. Dysbiosis in inflammatory bowel disease (IBD) has been implicated as a causal or contributory factor to the pathogenesis of the disease. This study, done on patients in remission while accounting for various confounding factors, shows significant community differences and altered community dynamics, even after acute inflammation has subsided. A cluster of was linked with Crohn's disease, suggesting that this cluster, which contains members known to disrupt colonization resistance and form biofilms, persists during quiescence and can lead to chronic inflammation. Flavonoid-degrading bacteria were also associated with IBD, raising the possibility that modification of dietary flavonoids might induce and maintain remission in IBD.
炎症性肠病(IBD)是一种慢性、复发性、炎症性疾病,包括两种主要疾病:克罗恩病(CD)和溃疡性结肠炎(UC)。尽管 IBD 的病因尚未完全阐明,但肠道微生物群被认为在其发展中起着至关重要的作用。本横断面研究旨在描述处于缓解期的 CD 或 UC 患者的粪便微生物群,以揭示维持残留炎症水平和引发疾病复发的潜在因素。招募了 98 名处于临床缓解期的 IBD 患者(66 名 UC,32 名 CD)和 97 名对照者,并收集了粪便样本和详细的患者数据。提取 DNA 后,扩增和测序 16S rRNA 基因的可变区 V1 和 V2。与健康对照组相比,IBD 患者的 alpha 多样性降低,beta 多样性指数显示两组之间存在差异。健康对照组与有益的未分类物种(unclassified species)(.)、.和.有关,而黄酮类降解细菌与 IBD 有关。网络分析确定了高度中心和有影响力的疾病标志物,以及一个与 IBD 强烈相关的网络模块,该模块可以作为维持和触发 IBD 的残留炎症过程的驱动力,即使在疾病活动度低的情况下也是如此。IBD 患者的微生物群与健康对照组明显不同,即使在缓解期也是如此,这表明微生物群是 IBD 慢性的重要驱动因素。炎症性肠病(IBD)中的菌群失调被认为是疾病发病机制的一个因果或促成因素。这项研究在考虑到各种混杂因素的情况下,对缓解期的患者进行研究,表明即使在急性炎症消退后,仍存在显著的群落差异和改变的群落动态。一个包含已知破坏定植抗性和形成生物膜的成员的 聚类与克罗恩病相关,这表明该聚类在静止期持续存在,并可能导致慢性炎症。黄酮类降解细菌也与 IBD 相关,这表明饮食中黄酮类化合物的修饰可能诱导和维持 IBD 的缓解。