Evidence map›Paper›PMID 33750910›Full record

ArticleCommunications biology2021

Non-responder phenotype reveals apparent microbiome-wide antibiotic tolerance in the murine gut.

Christian Diener, Anna C H Hoge, Sean M Kearney, Ulrike Kusebauch, Sushmita Patwardhan, Robert L Moritz, Susan E Erdman, Sean M Gibbons

Open access · goldAbstract readComparative Study
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 52% of its field
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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
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

8 authors at 4 institutions in 1 country.

Christian Diener *Institute for Systems Biology, Seattle, WA, USA.
Anna C H Hoge *Institute for Systems Biology, Seattle, WA, USA.
Sean M KearneyDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA, USA.
Ulrike KusebauchInstitute for Systems Biology, Seattle, WA, USA.
Sushmita PatwardhanInstitute for Systems Biology, Seattle, WA, USA.
Robert L MoritzInstitute for Systems Biology, Seattle, WA, USA.ORCID http://orcid.org/0000-0002-3216-9447
Susan E ErdmanDivision of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA, USA.
Sean M GibbonsInstitute for Systems Biology, Seattle, WA, USA. sgibbons@isbscience.org.ORCID http://orcid.org/0000-0002-8724-7916
Institute for Systems Biology · USBroad Institute · USMassachusetts Institute of Technology · USUniversity of Washington · US

Funding

Acquisition of Fusion Lumos Orbitrap mass spectrometerS10OD026936 · OD · INSTITUTE FOR SYSTEMS BIOLOGY · PI MORITZ, ROBERT L · 2019 to 2019
$600k
NIH HHS S10 OD026936
6 · The paper itself

Abstract

Broad spectrum antibiotics cause both transient and lasting damage to the ecology of the gut microbiome. Antibiotic-induced loss of gut bacterial diversity has been linked to susceptibility to enteric infections. Prior work on subtherapeutic antibiotic treatment in humans and non-human animals has suggested that entire gut communities may exhibit tolerance phenotypes. In this study, we validate the existence of these community tolerance phenotypes in the murine gut and explore how antibiotic treatment duration or a diet enriched in antimicrobial phytochemicals might influence the frequency of this phenotype. Almost a third of mice exhibited whole-community tolerance to a high dose of the β-lactam antibiotic cefoperazone, independent of antibiotic treatment duration or dietary phytochemical amendment. We observed few compositional differences between non-responder microbiota during antibiotic treatment and the untreated control microbiota. However, gene expression was vastly different between non-responder microbiota and controls during treatment, with non-responder communities showing an upregulation of antimicrobial tolerance genes, like efflux transporters, and a down-regulation of central metabolism. Future work should focus on what specific host- or microbiome-associated factors are responsible for tipping communities between responder and non-responder phenotypes so that we might learn to harness this phenomenon to protect our microbiota from routine antibiotic treatment.

Indexed as

Anti-Bacterial AgentsBacteriaCefoperazoneGastrointestinal MicrobiomeAnimal FeedAnimalsDrug Resistance, BacterialDysbiosisFecesFemaleGenotypeIntestinesMiceMice, Inbred C57BLPhenotypeSeaweedAnti-Bacterial AgentsCefoperazone

Identifiers

PMID33750910
PMCPMC7943787
OpenAlexW3134777992

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.