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结肠炎小鼠模型中口腔微生物群组成的变化。

Oral microbiome composition changes in mouse models of colitis.

作者信息

Rautava Jaana, Pinnell Lee J, Vong Linda, Akseer Nadia, Assa Amit, Sherman Philip M

机构信息

Cell Biology Program, Research Institute, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Oral Pathology and Oral Radiology, Institute of Dentistry, University of Turku, Turku, Finland.

出版信息

J Gastroenterol Hepatol. 2015 Mar;30(3):521-7. doi: 10.1111/jgh.12713.

Abstract

BACKGROUND AND AIM

Oral mucosal pathologies are frequent in inflammatory bowel disease (IBD). Since host-microbiome interactions are implicated in the pathogenesis of IBD, in this study the potential for changes affecting the oral microbiome was evaluated using two complementary mouse models of colitis: either chemically (dextran sulfate sodium) or with Citrobacter rodentium infection.

METHODS

After sacrifice, the tongue, buccal mucosa, saliva, colon, and stool samples were collected for analyses. Denaturing gradient gel electrophoresis was performed to assess bacterial 16S rRNA gene profiles. Relative changes were determined using quantitative polymerase chain reaction analysis for the phyla Bacteroidetes, Firmicutes, Spirochetes, and Actinobacteria, classes Gammaproteobacteria and Betaproteobacteria, and the genera Bacillus and Lactobacillus. These groups represent over 99% of the oral microbiota of healthy C57BL/6 mice.

RESULTS

Both models of colitis changed the oral microbiome, with the buccal microbiome being the most resistant to alterations in composition (maximum 1.8% change, vs tongue maximum 2.5% change, and saliva which demonstrated up to 7.2% total changes in microbiota composition). Changes in the oral microbiota were greater after dextran sulfate sodium challenge, compared with C. rodentium-induced colitis. Using cluster analysis, tongue and buccal mucosal microbiota composition changed ∼ 5%, saliva ∼ 35%, while stool changed ∼ 10%.

CONCLUSION

These findings indicate that dysbiosis observed in murine models of colitis is associated with changes in the composition of bacteria present in the oral cavity and in saliva. Such changes in the oral microbiota could be relevant to the etiology and management of oral mucosal pathologies observed in IBD patients.

摘要

背景与目的

口腔黏膜病变在炎症性肠病(IBD)中很常见。由于宿主-微生物群相互作用与IBD的发病机制有关,因此在本研究中,使用两种互补的结肠炎小鼠模型评估了影响口腔微生物群变化的可能性:化学诱导(葡聚糖硫酸钠)或啮齿柠檬酸杆菌感染。

方法

处死后,收集舌头、颊黏膜、唾液、结肠和粪便样本进行分析。进行变性梯度凝胶电泳以评估细菌16S rRNA基因谱。使用定量聚合酶链反应分析来确定拟杆菌门、厚壁菌门、螺旋体门和放线菌门、γ-变形菌纲和β-变形菌纲以及芽孢杆菌属和乳杆菌属的相对变化。这些菌群占健康C57BL/6小鼠口腔微生物群的99%以上。

结果

两种结肠炎模型均改变了口腔微生物群,其中颊部微生物群对组成变化的抵抗力最强(最大变化1.8%,而舌头最大变化2.5%,唾液微生物群组成的总变化高达7.2%)。与啮齿柠檬酸杆菌诱导的结肠炎相比,葡聚糖硫酸钠攻击后口腔微生物群的变化更大。使用聚类分析,舌头和颊黏膜微生物群组成变化约5%,唾液约35%,而粪便变化约10%。

结论

这些发现表明,在结肠炎小鼠模型中观察到的生态失调与口腔和唾液中细菌组成的变化有关。口腔微生物群的这种变化可能与IBD患者中观察到的口腔黏膜病变的病因和管理有关。

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