Evidence map›Paper›PMID 38698178›Full record

ArticleNature microbiology2024

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

Chen Liao, Thierry Rolling, Ana Djukovic, Teng Fei, Vishwas Mishra, Hongbin Liu, Chloe Lindberg, Lei Dai, Bing Zhai, Jonathan U Peled and 3 more

Abstract read
In one paragraph

Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Chen Liao *Program for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0001-8474-1196
Thierry Rolling *Infectious Disease Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Ana Djukovic *Program for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0001-8068-7188
Teng FeiDepartment of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0001-7888-1715
Vishwas MishraProgram for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Hongbin LiuCAS Key Laboratory of Quantitative Engineering Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Chloe LindbergProgram for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Lei DaiCAS Key Laboratory of Quantitative Engineering Biology, Shenzhen Institute of Synthetic Biology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.ORCID http://orcid.org/0000-0002-5598-5308
Bing ZhaiInfectious Disease Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0001-6571-7465
Jonathan U PeledAdult Bone Marrow Transplantation Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-4029-7625
Marcel R M van den BrinkAdult Bone Marrow Transplantation Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0003-0696-4401
Tobias M HohlInfectious Disease Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA. hohlt@mskcc.org.ORCID http://orcid.org/0000-0002-9097-5412
Joao B XavierProgram for Computational and Systems Biology, Memorial Sloan Kettering Cancer Center, New York, NY, USA. xavierj@mskcc.org.ORCID http://orcid.org/0000-0003-3592-1689

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Tumor-specific T cell state dynamics and heterogeneity in early tumorigenesisU54CA209975 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LESLIE, CHRISTINA S, RUDENSKY, ALEXANDER Y · 2016 to 2021
$11.8M
Systems Biology of Microbiome-mediated Resilience to Antibiotic-resistant PathogensU01AI124275 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI PAMER, ERIC G., XAVIER, JOAO · 2016 to 2020
$8.9M
INITIATION OF THE IMMUNE RESPONSE TO ASPERGILLUS FUMIGATUSR01AI093808 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI HOHL, TOBIAS M · 2011 to 2020
$4.9M
INITIATION OF THE IMMUNE RESPONSE TO ASPERGILLUS FUMIGATUSR37AI093808 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI TOBIAS M HOHL · 2021 to 2026
$4.2M
Mathematical ecology models of host-microbiota interaction in auto microbiota transplants (auto-FMT)R01AI137269 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI TAUR, YING, XAVIER, JOAO · 2019 to 2023
$3.8M
Antifungal Immunity and the Mechanism of Fungal Programmed Cell DeathR01AI139632 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI CRAMER, ROBERT ANDREW, HOHL, TOBIAS M · 2019 to 2023
$3.3M
Microbiota mechanisms and biomarkers in GVHDK08HL143189 · NHLBI · SLOAN-KETTERING INST CAN RESEARCH · PI PELED, JONATHAN · 2019 to 2023
$858k
The mycobiota, bone marrow transplantation, and clinical outcomesR21AI156157 · NIAID · SLOAN-KETTERING INST CAN RESEARCH · PI HOHL, TOBIAS M · 2021 to 2022
$487k
Deutsche Forschungsgemeinschaft (German Research Foundation) RO-5328/1-2 (T.R.)NCI NIH HHS P30 CA008748NCI NIH HHS U54 CA209975NHLBI NIH HHS K08 HL143189NIAID NIH HHS R01 AI093808NIAID NIH HHS R01 AI137269NIAID NIH HHS R01 AI139632NIAID NIH HHS R21 AI156157NIAID NIH HHS R37 AI093808NIAID NIH HHS U01 AI124275
6 · The paper itself

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.

Indexed as

BacteriaDysbiosisFecesGastrointestinal MicrobiomeMouthRNA, Ribosomal, 16SAnimalsAnti-Bacterial AgentsColitisDextran SulfateDisease Models, AnimalFemaleHumansInflammatory Bowel DiseasesMiceMice, Inbred C57BLAnti-Bacterial AgentsDextran SulfateRNA, Ribosomal, 16S

Identifiers

PMID38698178
PMCPMC11152985

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.