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粪便中口腔细菌的相对丰度因肠道微生物群耗竭而增加,并与患者的结果相关。

Oral bacteria relative abundance in faeces increases due to gut microbiota depletion and is linked with patient outcomes.

机构信息

Program for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Infectious Disease Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

出版信息

Nat Microbiol. 2024 Jun;9(6):1555-1565. doi: 10.1038/s41564-024-01680-3. Epub 2024 May 2.

DOI:10.1038/s41564-024-01680-3
PMID:38698178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11152985/
Abstract

The detection of oral bacteria in faecal samples has been associated with inflammation and intestinal diseases. The increased relative abundance of oral bacteria in faeces has two competing explanations: either oral bacteria invade the gut ecosystem and expand (the 'expansion' hypothesis), or oral bacteria transit through the gut and their relative increase marks the depletion of other gut bacteria (the 'marker' hypothesis). Here we collected oral and faecal samples from mouse models of gut dysbiosis (antibiotic treatment and DSS-induced colitis) and used 16S ribosomal RNA sequencing to determine the abundance dynamics of oral bacteria. We found that the relative, but not absolute, abundance of oral bacteria increases, reflecting the 'marker' hypothesis. Faecal microbiome datasets from diverse patient cohorts, including healthy individuals and patients with allogeneic haematopoietic cell transplantation or inflammatory bowel disease, consistently support the 'marker' hypothesis and explain associations between oral bacterial abundance and patient outcomes consistent with depleted gut microbiota. By distinguishing between the two hypotheses, our study guides the interpretation of microbiome compositional data and could potentially identify cases where therapies are needed to rebuild the resident microbiome rather than protect against invading oral bacteria.

摘要

粪便样本中口腔细菌的检测与炎症和肠道疾病有关。粪便中口腔细菌的相对丰度增加有两种相互竞争的解释:口腔细菌要么入侵肠道生态系统并扩张(“扩张”假说),要么口腔细菌通过肠道转运,其相对增加标志着其他肠道细菌的消耗(“标记”假说)。在这里,我们从肠道功能紊乱的小鼠模型(抗生素治疗和 DSS 诱导的结肠炎)中收集了口腔和粪便样本,并使用 16S 核糖体 RNA 测序来确定口腔细菌的丰度动态。我们发现,口腔细菌的相对丰度(而非绝对丰度)增加,反映了“标记”假说。来自不同患者队列(包括健康个体以及接受异基因造血细胞移植或炎症性肠病治疗的患者)的粪便微生物组数据集一致支持“标记”假说,并解释了口腔细菌丰度与患者预后之间的关联,这与消耗性肠道微生物组一致。通过区分这两种假说,我们的研究指导了对微生物组组成数据的解释,并可能有助于确定需要治疗以重建常驻微生物组而不是防止入侵口腔细菌的情况。

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