炎症性肠病
肠粘膜
拟杆菌
溃疡性结肠炎
粪便
生物
微生物群
胃肠病学
失调
微生物学
肠道菌群
结肠炎
疾病
内科学
医学
免疫学
细菌
生物信息学
遗传学
作者
David Schult,Christina Gassner,Niklas Thur,Chiara Hennig,Lisa Fricke,Lucia Liotta,Simon Weidlich,Monica Steffi Matchado,Bärbel Stecher,Leona Arps,Katja Steiger,Julius Shakhtour,Moritz Jesinghaus,Markus List,Klaus-Peter Janßen,Mohsen Pourjam,Klaus Neuhaus,Dirk Haller,Roland M. Schmid,Michael Quante
摘要
Abstract Background Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), is associated with changes in the gut microbiome. Studies comparing fecal, gut mucosal, and salivary microbiomes are rare, and questions remain regarding the interaction of these compartments. Methods In this case-control study, 16S rRNA gene amplicon sequencing was performed on samples from stool, intestinal mucosa, and saliva of 120 patients with IBD. Patients with signs of non-IBD colonic inflammation (N = 28) and healthy subjects (N = 67) served as controls. A total of 480 16S profiles were analyzed. The results were evaluated with multiple clinical and pathological parameters and potential confounders were considered. The study aimed to find microbial biomarkers specific to IBD and signatures of intestinal barrier dysfunction. Results Fecal α-diversity of IBD patients was reduced and Pseudomonas species was significantly increased in the mucosa of IBD patients (Pseudomonas-positive mucosa [PSM positive], P value < .001, Mann-Whitney U test). Comparison of matched stool and mucosa samples showed high abundance of Pseudomonas species in gut mucosa but not in fecal samples, especially in CD patients. Interestingly, in PSM positive, Paracoccus species, Bacteroides species, and Streptococcus species were more abundant. Importantly, the results were independent of disease severity, histopathology, medication, and other metadata. Conclusions The opportunistic pathogenic bacterium Pseudomonas species is more prevalent in the gut mucosa of patients with IBD. This indicates a disruption of the gut barrier with increasing mucosal colonization or invasion of the bacteria. The finding is independent of clinical metadata and confounders and occurs in new-onset IBD but not in non-IBD intestinal inflammation, which suggests disease specificity.
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